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Sample records for neurochemical deficits contribute

  1. Piperine Augments the Protective Effect of Curcumin Against Lipopolysaccharide-Induced Neurobehavioral and Neurochemical Deficits in Mice.

    Science.gov (United States)

    Jangra, Ashok; Kwatra, Mohit; Singh, Tavleen; Pant, Rajat; Kushwah, Pawan; Sharma, Yogita; Saroha, Babita; Datusalia, Ashok Kumar; Bezbaruah, Babul Kumar

    2016-06-01

    The aim of the present study was to investigate the protective effects of curcumin alone and in combination with piperine against lipopolysaccharide (LPS)-induced neurobehavioral and neurochemical deficits in the mice hippocampus. Mice were treated with curcumin (100, 200, and 400 mg/kg, p.o.) and piperine (20 mg/kg, p.o.) for 7 days followed by LPS (0.83 mg/kg, i.p.) administration. Animals exhibited anxiety and depressive-like phenotype after 3 and 24 h of LPS exposure, respectively. LPS administration increased the oxido-nitrosative stress as evident by elevated levels of malondialdehyde, nitrite, and depletion of glutathione level in the hippocampus. Furthermore, we found raised level of pro-inflammatory cytokines (IL-1β and TNF-α) in the hippocampus of LPS-treated mice. Pretreatment with curcumin alleviated LPS-induced neurobehavioral and neurochemical deficits. Furthermore, co-administration of curcumin with piperine significantly potentiated the neuroprotective effect of curcumin. These results demonstrate that piperine enhanced the neuroprotective effect of curcumin against LPS-induced neurobehavioral and neurochemical deficits.

  2. Treatment with Trehalose Prevents Behavioral and Neurochemical Deficits Produced in an AAV α-Synuclein Rat Model of Parkinson's Disease.

    Science.gov (United States)

    He, Qing; Koprich, James B; Wang, Ying; Yu, Wen-bo; Xiao, Bao-guo; Brotchie, Jonathan M; Wang, Jian

    2016-05-01

    The accumulation of misfolded α-synuclein in dopamine (DA) neurons is believed to be of major importance in the pathogenesis of Parkinson's disease (PD). Animal models of PD, based on viral-vector-mediated over-expression of α-synuclein, have been developed and show evidence of dopaminergic toxicity, providing us a good tool to investigate potential therapies to interfere with α-synuclein-mediated pathology. An efficient disease-modifying therapeutic molecule should be able to interfere with the neurotoxicity of α-synuclein aggregation. Our study highlighted the ability of an autophagy enhancer, trehalose (at concentrations of 5 and 2% in drinking water), to protect against A53T α-synuclein-mediated DA degeneration in an adeno-associated virus serotype 1/2 (AAV1/2)-based rat model of PD. Behavioral tests and neurochemical analysis demonstrated a significant attenuation in α-synuclein-mediated deficits in motor asymmetry and DA neurodegeneration including impaired DA neuronal survival and DA turnover, as well as α-synuclein accumulation and aggregation in the nigrostriatal system by commencing 5 and 2% trehalose at the same time as delivery of AAV. Trehalose (0.5%) was ineffective on the above behavioral and neurochemical deficits. Further investigation showed that trehalose enhanced autophagy in the striatum by increasing formation of LC3-II. This study supports the concept of using trehalose as a novel therapeutic strategy that might prevent/reverse α-synuclein aggregation for the treatment of PD.

  3. Neurochemical and electrical modulation of the Locus coeruleus: contribution to CO2 drive to breathe

    Directory of Open Access Journals (Sweden)

    Debora eDe Carvalho

    2014-08-01

    Full Text Available The Locus coeruleus (LC is a dorsal pontine region, situated bilaterally on the floor of the fourth ventricle. It is considered to be the major source of noradrenergic innervation in the brain. These neurons are highly sensitive to CO2 / pH, and chemical lesions of LC neurons largely attenuate the hypercapnic ventilatory response in unanesthetized adult rats. Developmental dysfunctions in these neurons are linked to pathological conditions such as Rett and sudden infant death syndromes, which can impair the control of the cardio-respiratory system. LC is densely innervated by fibers that contain glutamate, serotonin and ATP, and these neurotransmitters strongly affect LC activity, including central chemoreflexes. Aside from neurochemical modulation, LC neurons are also strongly electrically coupled, specifically through gap junctions, which play a role in the CO2 ventilatory response. This article reviews the available data on the role of chemical and electrical neuromodulation of the LC in the control of ventilation.

  4. Attenuation of neurobehavioral and neurochemical abnormalities in animal model of cognitive deficits of Alzheimer's disease by fermented soybean nanonutraceutical.

    Science.gov (United States)

    Bhatt, Prakash Chandra; Pathak, Shruti; Kumar, Vikas; Panda, Bibhu Prasad

    2018-02-01

    The present study was performed to evaluate the efficacy of nanonutraceuticals (NN) for attenuation of neurobehavioral and neurochemical abnormalities in Alzheimer's disease. Solid-state fermentation of soybean with Bacillus subtilis was performed to produce different metabolites (nattokinase, daidzin, genistin and glycitin and menaquinone-7). Intoxication of rats with colchicine caused impairment in learning and memory which was demonstrated in neurobehavioral paradigms (Morris water maze and passive avoidance) linked with decreased activity of acetylcholinesterase (AChE). NN treatment led to a significant increase in TLT in the retention trials as compared to acquisition trial TLT suggesting an improved learning and memory in rats. Further, treatment of NN caused an increase in the activity of AChE (42%), accompanied with a reduced activity of glutathione (42%), superoxide dismutase (43%) and catalase (41%). It also decreased the level of lipid peroxidation (28%) and protein carbonyl contents (30%) in hippocampus as compared to those treated with colchicine alone, suggesting a possible neuroprotective efficacy of NN. Interestingly, in silico studies also demonstrated an effective amyloid-β and BACE-1 inhibition activity. These findings clearly indicated that NN reversed colchicine-induced behavioral and neurochemical alterations through potent antioxidant activity and could possibly impart beneficial effects in cognitive defects associated with Alzheimer's disease.

  5. The DYX2 locus and neurochemical signaling genes contribute to speech sound disorder and related neurocognitive domains.

    Science.gov (United States)

    Eicher, J D; Stein, C M; Deng, F; Ciesla, A A; Powers, N R; Boada, R; Smith, S D; Pennington, B F; Iyengar, S K; Lewis, B A; Gruen, J R

    2015-04-01

    A major milestone of child development is the acquisition and use of speech and language. Communication disorders, including speech sound disorder (SSD), can impair a child's academic, social and behavioral development. Speech sound disorder is a complex, polygenic trait with a substantial genetic component. However, specific genes that contribute to SSD remain largely unknown. To identify associated genes, we assessed the association of the DYX2 dyslexia risk locus and markers in neurochemical signaling genes (e.g., nicotinic and dopaminergic) with SSD and related endophenotypes. We first performed separate primary associations in two independent samples - Cleveland SSD (210 affected and 257 unaffected individuals in 127 families) and Denver SSD (113 affected individuals and 106 unaffected individuals in 85 families) - and then combined results by meta-analysis. DYX2 markers, specifically those in the 3' untranslated region of DCDC2 (P = 1.43 × 10(-4) ), showed the strongest associations with phonological awareness. We also observed suggestive associations of dopaminergic-related genes ANKK1 (P = 1.02 × 10(-2) ) and DRD2 (P = 9.22 × 10(-3) ) and nicotinic-related genes CHRNA3 (P = 2.51 × 10(-3) ) and BDNF (P = 8.14 × 10(-3) ) with case-control status and articulation. Our results further implicate variation in putative regulatory regions in the DYX2 locus, particularly in DCDC2, influencing language and cognitive traits. The results also support previous studies implicating variation in dopaminergic and nicotinic neural signaling influencing human communication and cognitive development. Our findings expand the literature showing genetic factors (e.g., DYX2) contributing to multiple related, yet distinct neurocognitive domains (e.g., dyslexia, language impairment, and SSD). How these factors interactively yield different neurocognitive and language-related outcomes remains to be elucidated. © 2015 The Authors. Genes, Brain and Behavior published by

  6. Executive and attentional contributions to Theory of Mind deficit in attention deficit/hyperactivity disorder (ADHD).

    Science.gov (United States)

    Mary, Alison; Slama, Hichem; Mousty, Philippe; Massat, Isabelle; Capiau, Tatiana; Drabs, Virginie; Peigneux, Philippe

    2016-01-01

    Attention deficit/hyperactivity disorder (ADHD) in children has been associated with attentional and executive problems, but also with socioemotional difficulties possibly associated with deficits in Theory of Mind (ToM). Socioemotional problems in ADHD are associated with more negative prognoses, notably interpersonal, educational problems, and an increased risk of developing other psychiatric disorders that emphasize the need to clarify the nature of their ToM deficits. In this study, we hypothesized that ToM dysfunction in children with ADHD is largely attributable to their attentional and/or executive deficits. Thirty-one children with ADHD (8-12 years, IQ > 85) and 31 typically developing (TD) children were assessed using executive functions (inhibition, planning, and flexibility) and attentional tasks, as well as two advanced ToM tasks (Reading the Mind in the Eyes and Faux Pas) involving different levels of executive control. Children with ADHD performed more poorly than TD children in attentional, executive function, and ToM tasks. Linear regression analyses conducted in the ADHD group indicated that inhibition scores predicted performance on the "Faux Pas" task the best, while attention scores were the best for predicting performance on the Reading the Mind in the Eyes task. When controlled for inhibition and attentional variables, ToM performance in children with ADHD was actually similar to TD children. Contrarily, controlling for ToM scores did not normalize performance for inhibition and attentional tasks in children with ADHD. This unidirectional relationship suggests that deficits in the EF and attentional domains are responsible for ToM deficits in ADHD, which therefore may contribute to their socioemotional difficulties.

  7. Mechanisms contributing to cognitive deficits in cannabis users.

    Science.gov (United States)

    Mizrahi, Romina; Watts, Jeremy J; Tseng, Kuei Y

    2017-09-15

    Studies from preclinical animal models indicate that sustained activation of CB1 receptor signaling is a major contributing factor for the onset of cognitive deficits associated to chronic cannabis use, in particular within the working memory and decision-making domains. Yet, very few studies have been designed to directly assess the role of CB1 receptors in mediating the effects of cannabis on human brain function. This perspective review article provides an overview of current state of knowledge on possible neurobiological mechanisms accounting for the detrimental effects of chronic cannabis use on cognition and related changes in brain structure and functional connectivity. This article is part of the Special Issue entitled "A New Dawn in Cannabinoid Neurobiology". Copyright © 2017 Elsevier Ltd. All rights reserved.

  8. Attention Contributes to Arithmetic Deficits in New-Onset Childhood Absence Epilepsy

    Directory of Open Access Journals (Sweden)

    Dazhi Cheng

    2017-09-01

    Full Text Available Neuropsychological studies indicate that new-onset childhood absence epilepsy (CAE is associated with deficits in attention and executive functioning. However, the contribution of these deficits to impaired academic performance remains unclear. We aimed to examine whether attention and executive functioning deficits account for the academic difficulties prevalent in patients with new-onset CAE. We analyzed cognitive performance in several domains, including language, mathematics, psychomotor speed, spatial ability, memory, general intelligence, attention, and executive functioning, in 35 children with new-onset CAE and 33 control participants. Patients with new-onset CAE exhibited deficits in mathematics, general intelligence, attention, and executive functioning. Furthermore, attention deficits, as measured by a visual tracing task, accounted for impaired arithmetic performance in the new-onset CAE group. Therefore, attention deficits, rather than impaired general intelligence or executive functioning, may be responsible for arithmetic performance deficits in patients with new-onset CAE.

  9. The Contribution of Deficits in Emotional Clarity to Stress Responses and Depression

    Science.gov (United States)

    Flynn, Megan; Rudolph, Karen D.

    2010-01-01

    This research investigated the contribution of deficits in emotional clarity to children's socioemotional adjustment. Specifically, this study examined the proposal that deficits in emotional clarity are associated with maladaptive interpersonal stress responses, and that maladaptive interpersonal stress responses act as a mechanism linking…

  10. Neural Deficits Contribute to Respiratory Insufficiency in Pompe Disease

    National Research Council Canada - National Science Library

    Lara R. DeRuisseau; David D. Fuller; Kai Qiu; Keith C. DeRuisseau; William H. Donnelly; Cathryn Mah; Paul J. Reier; Barry J. Byrne; Kenneth I. Berns

    2009-01-01

    .... Respiratory dysfunction is a hallmark of the disease, muscle weakness has been viewed as the underlying cause, and the possibility of an associated neural contribution has not been evaluated previously...

  11. Neurochemical aspects of childhood autism

    NARCIS (Netherlands)

    R.B. Minderaa (Ruud)

    1985-01-01

    textabstractThe topic of this thesis is neurochemical aspects of infantile autism. The experimental work is centered around the most robust and consistant neurochemical finding in child psychiatry, namely that group mean whole blood serotonin (5-Hydroxytryptamine, 5-HT) values are

  12. Deficit

    CERN Multimedia

    2002-01-01

    UCL's former provost, Sir Derek Roberts, has been drafted in for a year to run the college. UCL is expected to have a 6 million pounds deficit this year and up to a 10 million pounds deficit next year. Sir Christopher Llewellyn-Smith took over at UCL nearly 4 years ago and decided then that the finanical situation was serious enough to warrant a reduction in the vast expansion policy undertaken by his predecessor (1 page).

  13. Suicide: Neurochemical Approaches

    Directory of Open Access Journals (Sweden)

    Ritabrata Banerjee

    2013-10-01

    Full Text Available Despite the devastating effect of suicide on numerous lives, there is still a dearthof knowledge concerning its neurochemical aspects. There is increasing evidence that brain-derived neurotrophic factor (BDNF and Nerve growth factor (NGF are involved in the pathophysiology and treatment of depression through binding and activating their cognate receptors trk B and trk A respectively. The present study was performed to examine whether the expression profiles of BDNF and/or trk B as well as NGF and/or trk A were altered in postmortem brain in subjects who commitsuicide and whether these alterations were associated with specific psychopathologic conditions. These studies were performed in hippocampus obtained 21 suicide subjects and 19 non-psychiatric control subjects. The protein and mRNA levels of BDNF, trk B and NGF, trk A were determined with Sandwich ELISA, Western Blot and RT PCR respectively. Given the importance of BDNFand NGF along with their cognate receptors in mediating physiological functions, including cell survival and synaptic plasticity, our findings of reduced expression of BDNF, Trk B and NGF, Trk A in both protein and mRNA levels of postmortem brain in suicide subjects suggest that these molecules may play an important role in the pathophysiological aspects of suicidal behavior.

  14. Physiological mechanisms contributing to the increased water-use efficiency in winter wheat under deficit irrigation.

    Science.gov (United States)

    Xue, Qingwu; Zhu, Zixi; Musick, Jack T; Stewart, B A; Dusek, Donald A

    2006-02-01

    Deficit irrigation in winter wheat has been practiced in the areas with limited irrigation water resources. The objectives of this study were to (i) understand the physiological basis for determinations of grain yield and water-use efficiency in grain yield (WUE) under deficit irrigation; and (ii) investigate the effect of deficit irrigation on dry matter accumulation and remobilization of pre-anthesis carbon reserves during grain filling. A field experiment was conducted in the Southern High Plains of the USA and winter wheat (cv. TAM 202) was grown on Pullman clay loam soil (fine mixed thermic Torretic Paleustoll). Treatments consisted of rain-fed, deficit irrigation from jointing to the middle of grain filling, and full irrigation. The physiological measurements included leaf water potential, net photosynthetic rate (Pn), stomatal conductance (Gs), and leaf area index. The rain-fed treatment had the lowest seasonal evapotranspiration (ET), biomass, grain yield, harvest index (HI) and WUE as a result of moderate to severe water stress from jointing to grain filling. Irrigation application increased seasonal ET, and ET increased as irrigation frequency increased. The seasonal ET increased 20% in one-irrigation treatments between jointing and anthesis, 32-46% in two-irrigation treatments, and 67% in three- and full irrigation treatments. Plant biomass, grain yield, HI and WUE increased as the result of increased ET. The increased yield under irrigation was mainly contributed by the increased number of spikes, and seeds per square meter and per spike. Among the irrigation treatments, grain yield increased significantly but the WUE increased slightly as irrigation frequency increased. The increased WUE under deficit irrigation was contributed by increased HI. Water stress during grain filling reduced Pn and Gs, and accelerated leaf senescence. However, the water stress during grain filling induced remobilization of pre-anthesis carbon reserves to grains, and the

  15. Alcohol-related amnesia and dementia: Animal models have revealed the contributions of different etiological factors on neuropathology, neurochemical dysfunction and cognitive impairment

    Science.gov (United States)

    Vetreno, Ryan P.; Hall, Joseph M.; Savage, Lisa M.

    2011-01-01

    Chronic alcoholism is associated with impaired cognitive functioning. Over 75% of autopsied chronic alcoholics have significant brain damage and over 50% of detoxified alcoholics display some degree of learning and memory impairment. However, the relative contributions of different etiological factors to the development of alcohol-related neuropathology and cognitive impairment are questioned. One reason for this quandary is that both alcohol toxicity and thiamine deficiency result in brain damage and cognitive problems. Two alcohol-related neurological disorders, alcohol-associated dementia and Wernicke-Korsakoff syndrome have been modeled in rodents. These pre-clinical models have elucidated the relative contributions of ethanol toxicity and thiamine deficiency to the development of dementia and amnesia. What is observed in these models—from repeated and chronic ethanol exposure to thiamine deficiency—is a progression of both neural and cognitive dysregulation. Repeated binge exposure to ethanol leads to changes in neural plasticity by reducing GABAergic inhibition and facilitating glutamatergic excitation, long-term chronic ethanol exposure results in hippocampal and cortical cell loss as well as reduced hippocampal neurotrophin protein content critical for neural survival, and thiamine deficiency results in gross pathological lesions in the diencephalon, reduced neurotrophic protein levels, and neurotransmitters levels in the hippocampus and cortex. Behaviorally, after recovery from repeated or chronic ethanol exposure there is impairment in working or episodic memory that can recover with prolonged abstinence. In contrast, after thiamine deficiency there is severe and persistent spatial memory impairments and increased perseverative behavior. The interaction between ethanol and thiamine deficiency does not produce more behavioral or neural pathology, with the exception of reduction of white matter, than long-term thiamine deficiency alone. PMID:21256970

  16. Less efficient pattern separation may contribute to age-related spatial memory deficits

    Directory of Open Access Journals (Sweden)

    Heather M. Holden

    2012-05-01

    Full Text Available Spatial memory deficits have been well documented in older adults and may serve as an early indicator of mild cognitive impairment or Alzheimer’s disease in some individuals. Pattern separation is a critical mechanism for reducing potential interference among similar memory representations to enhance memory accuracy. A small but growing literature indicates that spatial pattern separation may become less efficient as a result of normal aging, possibly due to age-related changes in subregions of the hippocampus. This decreased efficiency in spatial pattern separation may be a critical processing deficit that could be a contributing factor to spatial memory deficits and episodic memory impairment associated with aging. The present paper will review recently published studies in humans, nonhuman primates, and rodents that have examined age-related changes in spatial pattern separation. The potential basic science, translational, and clinical implications from these studies are discussed to illustrate the need for future research to further examine the relationship between spatial pattern separation and brain changes associated with aging and neurodegenerative disease.

  17. Mitochondrial Superoxide Contributes to Hippocampal Synaptic Dysfunction and Memory Deficits in Angelman Syndrome Model Mice.

    Science.gov (United States)

    Santini, Emanuela; Turner, Kathryn L; Ramaraj, Akila B; Murphy, Michael P; Klann, Eric; Kaphzan, Hanoch

    2015-12-09

    Angelman syndrome (AS) is a neurodevelopmental disorder associated with developmental delay, lack of speech, motor dysfunction, and epilepsy. In the majority of the patients, AS is caused by the deletion of small portions of maternal chromosome 15 harboring the UBE3A gene. This results in a lack of expression of the UBE3A gene because the paternal allele is genetically imprinted. The UBE3A gene encodes an enzyme termed ubiquitin ligase E3A (E6-AP) that targets proteins for degradation by the 26S proteasome. Because neurodegenerative disease and other neurodevelopmental disorders have been linked to oxidative stress, we asked whether mitochondrial reactive oxygen species (ROS) played a role in impaired synaptic plasticity and memory deficits exhibited by AS model mice. We discovered that AS mice have increased levels of superoxide in area CA1 of the hippocampus that is reduced by MitoQ 10-methanesuflonate (MitoQ), a mitochondria-specific antioxidant. In addition, we found that MitoQ rescued impairments in hippocampal synaptic plasticity and deficits in contextual fear memory exhibited by AS model mice. Our findings suggest that mitochondria-derived oxidative stress contributes to hippocampal pathophysiology in AS model mice and that targeting mitochondrial ROS pharmacologically could benefit individuals with AS. Oxidative stress has been hypothesized to contribute to the pathophysiology of neurodevelopmental disorders, including autism spectrum disorders and Angelman syndrome (AS). Herein, we report that AS model mice exhibit elevated levels of mitochondria-derived reactive oxygen species in pyramidal neurons in hippocampal area CA1. Moreover, we demonstrate that the administration of MitoQ (MitoQ 10-methanesuflonate), a mitochondria-specific antioxidant, to AS model mice normalizes synaptic plasticity and restores memory. Finally, our findings suggest that antioxidants that target the mitochondria could be used therapeutically to ameliorate synaptic and cognitive

  18. Anaerobic contribution during maximal anaerobic running test: correlation with maximal accumulated oxygen deficit.

    Science.gov (United States)

    Zagatto, A; Redkva, P; Loures, J; Kalva Filho, C; Franco, V; Kaminagakura, E; Papoti, M

    2011-12-01

    The aims of this study were: (i) to measure energy system contributions in maximal anaerobic running test (MART); and (ii) to verify any correlation between MART and maximal accumulated oxygen deficit (MAOD). Eleven members of the armed forces were recruited for this study. Participants performed MART and MAOD, both accomplished on a treadmill. MART consisted of intermittent exercise, 20 s effort with 100 s recovery, after each spell of effort exercise. Energy system contributions by MART were also determined by excess post-exercise oxygen consumption, lactate response, and oxygen uptake measurements. MAOD was determined by five submaximal intensities and one supramaximal intensity exercises corresponding to 120% at maximal oxygen uptake intensity. Energy system contributions were 65.4±1.1% to aerobic; 29.5±1.1% to anaerobic a-lactic; and 5.1±0.5% to anaerobic lactic system throughout the whole test, while only during effort periods the anaerobic contribution corresponded to 73.5±1.0%. Maximal power found in MART corresponded to 111.25±1.33 mL/kg/min but did not significantly correlate with MAOD (4.69±0.30 L and 70.85±4.73 mL/kg). We concluded that the anaerobic a-lactic system is the main energy system in MART efforts and this test did not significantly correlate to MAOD. © 2011 John Wiley & Sons A/S.

  19. Contribution of animal models to contemporary understanding of Attention Deficit Hyperactivity Disorder.

    Science.gov (United States)

    Carvalho, Constança; Vieira Crespo, Mariana; Ferreira Bastos, Luisa; Knight, Andrew; Vicente, Luís

    2016-01-01

    Attention Deficit Hyperactivity Disorder (ADHD) is a poorly understood neurodevelopmental disorder of multifactorial origin. Animal-based research has been used to investigate ADHD aetiology, pathogenesis and treatment, but the efficacy of this research for patients has not yet been systematically evaluated. However, such evaluation is important, given the resource consumption and ethical concerns incurred by animal use. Accordingly, we used the citation tracking facility within Web of Science to locate original research performed on animal models related to ADHD, prior to 2010. Human medical papers citing those animal studies were carefully analyzed by two independent raters to evaluate the contribution of the animal to the human studies. 211 publications describing relevant animal studies were located. Approximately half (3,342) of their 6,406 citations were by other animal studies. 446 human medical papers cited 121 of these 211 animal studies, a total of 500 times. 254 of these 446 papers were human studies of ADHD. However, only eight animal papers (cited 10 times) were relevant to the hypothesis of the human medical study in question. Three of these eight papers described results from both human and animal studies, but their citations solely referred to the human data. Five animal research papers were relevant to the hypotheses of the applicable human medical papers. Citation analysis indicates that animal research has contributed very little to contemporary understanding of ADHD. To ensure optimal allocation of Research & Development funds targeting this disease the contribution of other research methods should be similarly evaluated.

  20. Prior Methamphetamine Self-Administration Attenuates the Dopaminergic Deficits Caused by a Subsequent Methamphetamine Exposure

    OpenAIRE

    McFadden, Lisa M.; Vieira-Brock, Paula L.; Hanson, Glen R.; Fleckenstein, Annette E.

    2015-01-01

    Others and we have reported that prior methamphetamine (METH) exposure attenuates the persistent striatal dopaminergic deficits caused by a subsequent high-dose “binge” METH exposure. The current study investigated intermediate neurochemical changes that may contribute to, or serve to predict, this resistance. Rats self-administered METH or saline for 7 d. On the following day (specifically, 16 h after the conclusion of the final METH self-administration session), rats received a binge exposu...

  1. Age-Related Neurochemical Changes in the Vestibular Nuclei

    Directory of Open Access Journals (Sweden)

    Paul eSmith

    2016-03-01

    Full Text Available There is evidence that the normal aging process is associated with impaired vestibulo-ocular (VOR and vestibulo-spinal reflexes, causing reduced visual acuity and postural instability. Nonetheless, the available evidence is not entirely consistent, especially with respect to the VOR. Some recent studies have reported that VOR gain can be intact even above 80 years of age. Similarly, although there is evidence for age-related hair cell loss and neuronal loss in Scarpa’s ganglion and the vestibular nucleus complex (VNC, it is not entirely consistent. Whatever structural and functional changes occur in the VNC as a result of aging, either to cause vestibular impairment or to compensate for it, neurochemical changes must underlie them. However, the neurochemical changes that occur in the VNC with aging are poorly understood because the available literature is very limited. This review summarises and critically evaluates the available evidence relating to the noradrenaline, serotonin, dopamine, glutamate, GABA, glycine, and nitric oxide neurotransmitter systems in the aging VNC. It is concluded that, at present, it is difficult, if not impossible, to relate the neurochemical changes observed to the function of specific VNC neurons and whether the observed changes are the cause of a functional deficit in the VNC or an effect of it. A better understanding of the neurochemical changes that occur during aging may be important for the development of potential drug treatments for age-related vestibular disorders. However, this will require the use of more sophisticated methodology such as in vivo microdialysis with single neuron recording and perhaps new technologies such as optogenetics.

  2. Age-Related Neurochemical Changes in the Vestibular Nuclei.

    Science.gov (United States)

    Smith, Paul F

    2016-01-01

    There is evidence that the normal aging process is associated with impaired vestibulo-ocular reflexes (VOR) and vestibulo-spinal reflexes, causing reduced visual acuity and postural instability. Nonetheless, the available evidence is not entirely consistent, especially with respect to the VOR. Some recent studies have reported that VOR gain can be intact even above 80 years of age. Similarly, although there is evidence for age-related hair cell loss and neuronal loss in Scarpa's ganglion and the vestibular nucleus complex (VNC), it is not entirely consistent. Whatever structural and functional changes occur in the VNC as a result of aging, either to cause vestibular impairment or to compensate for it, neurochemical changes must underlie them. However, the neurochemical changes that occur in the VNC with aging are poorly understood because the available literature is very limited. This review summarizes and critically evaluates the available evidence relating to the noradrenaline, serotonin, dopamine, glutamate, GABA, glycine, and nitric oxide neurotransmitter systems in the aging VNC. It is concluded that, at present, it is difficult, if not impossible, to relate the neurochemical changes observed to the function of specific VNC neurons and whether the observed changes are the cause of a functional deficit in the VNC or an effect of it. A better understanding of the neurochemical changes that occur during aging may be important for the development of potential drug treatments for age-related vestibular disorders. However, this will require the use of more sophisticated methodology such as in vivo microdialysis with single neuron recording and perhaps new technologies such as optogenetics.

  3. Contributions from specific and general factors to unique deficits: two cases of mathematics learning difficulties.

    Science.gov (United States)

    Haase, Vitor G; Júlio-Costa, Annelise; Lopes-Silva, Júlia B; Starling-Alves, Isabella; Antunes, Andressa M; Pinheiro-Chagas, Pedro; Wood, Guilherme

    2014-01-01

    Mathematics learning difficulties are a highly comorbid and heterogeneous set of disorders linked to several dissociable mechanisms and endophenotypes. Two of these endophenotypes consist of primary deficits in number sense and verbal numerical representations. However, currently acknowledged endophenotypes are underspecified regarding the role of automatic vs. controlled information processing, and their description should be complemented. Two children with specific deficits in number sense and verbal numerical representations and normal or above-normal intelligence and preserved visuospatial cognition illustrate this point. Child H.V. exhibited deficits in number sense and fact retrieval. Child G.A. presented severe deficits in orally presented problems and transcoding tasks. A partial confirmation of the two endophenotypes that relate to the number sense and verbal processing was obtained, but a much more clear differentiation between the deficits presented by H.V. and G.A. can be reached by looking at differential impairments in modes of processing. H.V. is notably competent in the use of controlled processing but has problems with more automatic processes, such as nonsymbolic magnitude processing, speeded counting and fact retrieval. In contrast, G.A. can retrieve facts and process nonsymbolic magnitudes but exhibits severe impairment in recruiting executive functions and the concentration that is necessary to accomplish transcoding tasks and word problem solving. These results indicate that typical endophenotypes might be insufficient to describe accurately the deficits that are observed in children with mathematics learning abilities. However, by incorporating domain-specificity and modes of processing into the assessment of the endophenotypes, individual deficit profiles can be much more accurately described. This process calls for further specification of the endophenotypes in mathematics learning difficulties.

  4. Contributions from specific and general factors to unique deficits: two cases of mathematics learning difficulties

    Directory of Open Access Journals (Sweden)

    Vitor Geraldi Haase

    2014-02-01

    Full Text Available Mathematics learning difficulties are a highly comorbid and heterogeneous set of disorders linked to several dissociable mechanisms and endophenotypes. Two of these endophenotypes consist of primary deficits in number sense and verbal numerical representations. However, currently acknowledged endophenotypes are underspecified regarding the role of automatic vs. controlled information processing, and their description should be complemented. Two children with specific deficits in number sense and verbal numerical representations and normal or above-normal intelligence and preserved visuospatial cognition illustrate this point. Child H.V. exhibited deficits in number sense and fact retrieval. Child G.A. presented severe deficits in orally presented problems and transcoding tasks. A partial confirmation of the two endophenotypes that relate to the number sense and verbal processing was obtained, but a much more clear differentiation between the deficits presented by H.V. and G.A. can be reached by looking at differential impairments in modes of processing. H.V. is notably competent in the use of controlled processing but has problems with more automatic processes, such as nonsymbolic magnitude processing, speeded counting and fact retrieval. In contrast, G.A. can retrieve facts and process nonsymbolic magnitudes but exhibits severe impairment in recruiting executive functions and the concentration that is necessary to accomplish transcoding tasks and word problem solving. These results indicate that typical endophenotypes might be insufficient to describe accurately the deficits that are observed in children with mathematics learning abilities. However, by incorporating domain-specificity and modes of processing into the assessment of the endophenotypes, individual deficit profiles can be much more accurately described. This process calls for further specification of the endophenotypes in mathematics learning difficulties.

  5. Contributions from specific and general factors to unique deficits: two cases of mathematics learning difficulties

    Science.gov (United States)

    Haase, Vitor G.; Júlio-Costa, Annelise; Lopes-Silva, Júlia B.; Starling-Alves, Isabella; Antunes, Andressa M.; Pinheiro-Chagas, Pedro; Wood, Guilherme

    2014-01-01

    Mathematics learning difficulties are a highly comorbid and heterogeneous set of disorders linked to several dissociable mechanisms and endophenotypes. Two of these endophenotypes consist of primary deficits in number sense and verbal numerical representations. However, currently acknowledged endophenotypes are underspecified regarding the role of automatic vs. controlled information processing, and their description should be complemented. Two children with specific deficits in number sense and verbal numerical representations and normal or above-normal intelligence and preserved visuospatial cognition illustrate this point. Child H.V. exhibited deficits in number sense and fact retrieval. Child G.A. presented severe deficits in orally presented problems and transcoding tasks. A partial confirmation of the two endophenotypes that relate to the number sense and verbal processing was obtained, but a much more clear differentiation between the deficits presented by H.V. and G.A. can be reached by looking at differential impairments in modes of processing. H.V. is notably competent in the use of controlled processing but has problems with more automatic processes, such as nonsymbolic magnitude processing, speeded counting and fact retrieval. In contrast, G.A. can retrieve facts and process nonsymbolic magnitudes but exhibits severe impairment in recruiting executive functions and the concentration that is necessary to accomplish transcoding tasks and word problem solving. These results indicate that typical endophenotypes might be insufficient to describe accurately the deficits that are observed in children with mathematics learning abilities. However, by incorporating domain-specificity and modes of processing into the assessment of the endophenotypes, individual deficit profiles can be much more accurately described. This process calls for further specification of the endophenotypes in mathematics learning difficulties. PMID:24592243

  6. Reduced short-term memory span in aphasia and susceptibility to interference: contribution of material-specific maintenance deficits.

    Science.gov (United States)

    Barde, Laura H F; Schwartz, Myrna F; Chrysikou, Evangelia G; Thompson-Schill, Sharon L

    2010-03-01

    Semantic short-term memory (STM) deficits have been traditionally defined as an inability to maintain semantic representations over a delay (Martin et al., 1994b). Yet some patients with semantic STM deficits make numerous intrusions of items from previously presented lists, thus presenting an interesting paradox: why should an inability to maintain semantic representations produce an increase in intrusions from earlier lists? In this study, we investigated the relationship between maintenance deficits and susceptibility to interference in a group of 20 aphasic patients characterized with weak semantic or weak phonological STM. Patients and matched control participants performed a modified item-recognition task designed to elicit semantic or phonological interference from list items located one, two, or three trials back (Hamilton & Martin, 2007). Controls demonstrated significant effects of interference in both versions of the task. Interference in patients was predicted by the type and severity of their STM deficit; that is, shorter semantic spans were associated with greater semantic interference and shorter phonological spans were associated with greater phonological interference. We interpret these results through a new perspective, the reactivation hypothesis, and we discuss their importance for accounts emphasizing the contribution of maintenance mechanisms for STM impairments in aphasia as well as susceptibility to interference. Copyright (c) 2009 Elsevier Ltd. All rights reserved.

  7. Understanding How Social and Emotional Skill Deficits Contribute to School Failure

    Science.gov (United States)

    Whitted, Kathryn S.

    2011-01-01

    A growing number of children are entering kindergarten without the skills that enable them to be successful in an academic setting. However, it is not children's cognitive skills that concern educators; it is their social and emotional skill deficits that are most troublesome. This article discusses how family and community risk factors can…

  8. In vivo effect of chronic hypoxia on the neurochemical profile of the developing rat hippocampus

    OpenAIRE

    Raman, Lakshmi; Tkac, Ivan; Ennis, Kathleen; Georgieff, Michael K.; Gruetter, Rolf; Rao, Raghavendra

    2005-01-01

    The cognitive deficits observed in children with cyanotic congenital heart disease suggest involvement of the developing hippocampus. Chronic postnatal hypoxia present during infancy in these children may play a role in these impairments. To understand the biochemical mechanisms of hippocampal injury in chronic hypoxia, a neurochemical profile consisting of 15 metabolite concentrations and 2 metabolite ratios in the hippocampus was evaluated in a rat model of chronic postnatal hypoxia using i...

  9. Simultaneous wireless electrophysiological and neurochemical monitoring

    Science.gov (United States)

    Murari, Kartikeya; Mollazadeh, Mohsen; Thakor, Nitish; Cauwenberghs, Gert

    2008-08-01

    Information processing and propagation in the central nervous system is mostly electrical in nature. At synapses, electrical signals cause the release of neurotransmitters like dopamine, glutamate etc., that are sensed by post-synaptic neurons resulting in signal propagation or inhibition. It can be very informative to monitor electrical and neurochemical signals simultaneously to understand the mechanisms underlying normal or abnormal brain function. We present an integrated system for the simultaneous wireless acquisition of neurophysiological and neurochemical activity. Applications of the system to neuroscience include monitoring EEG and glutamate in rat somatosensory cortex following global ischemia.

  10. Is lack of breakfast contributing to nutrient deficits and poor nutritional indicators among adolescent girls?

    Science.gov (United States)

    Jeyakumar, Angeline; Ghugre, Padmini

    2017-09-01

    Breakfast is considered the first and most important meal of the day. Missing the first meal may result in significant nutritional deficits, if not compensated in subsequent meals. To describe the nutrient intake through breakfast and to study its association with nutritional indicators among adolescent girls. A cross-sectional study among adolescent girls ( n = 565) 16-18 years was carried out in urban slums of Pune, Maharashtra, India. Haemoglobin was assessed by cyanmethemoglobin method. Nutritional status was assessed through anthropometry and three 24-hours diet recall. Z scores, independent sample test, and linear logistic regression were used to assess undernutrition, to compare means of nutrient intake and to associate nutrient intake with nutritional status, respectively. Almost 50% did not consume solid food for breakfast and 99% of the participants consumed inadequate breakfast (breakfast emerged: I (bakery products + beverage) and II (traditional breakfast + beverage). Although the mean energy intake of type II breakfast (235±100.55 kcal) and the mean micronutrient intake was significantly higher than type I (micronutrients: vitamin C and folate ( p = 0.001), iron ( p = 0.01)) it did not meet the adequacy norms for breakfast. Among nutritional indicators breakfast intake was not directly associated with body mass index. However, mean intake of nutrients such as energy, protein and iron through the day were significantly lesser ( p = 0.001, p = 0.01 and p = 0.01 respectively) among anaemic adolescents. Linear regression showed significant association between energy, fat intake and BAZ scores. Compensating dietary deficits that arise in the first meal would directly address the day's nutrient deficit. The results highlight the need for a food-based approach to address undernutrition among adolescent girls in resource-poor settings.

  11. Mitochondrial Superoxide Contributes to Blood Flow and Axonal Transport Deficits in the Tg2576 Mouse Model of Alzheimer's Disease

    Science.gov (United States)

    Massaad, Cynthia A.; Amin, Samir K.; Hu, Lingyun; Mei, Yuan

    2010-01-01

    Background Alzheimer's disease (AD) is a neurodegenerative disease characterized by the progressive decline in cognitive functions and the deposition of aggregated amyloid β (Aβ) into senile plaques and the protein tau into tangles. In addition, a general state of oxidation has long been known to be a major hallmark of the disease. What is not known however, are the mechanisms by which oxidative stress contributes to the pathology of AD. Methodology/Principal Findings In the current study, we used a mouse model of AD and genetically boosted its ability to quench free radicals of specific mitochondrial origin. We found that such manipulation conferred to the AD mice protection against vascular as well as neuronal deficits that typically affect them. We also found that the vascular deficits are improved via antioxidant modulation of the endothelial nitric oxide synthase, an enzyme primarily responsible for the production of nitric oxide, while neuronal deficits are improved via modulation of the phosphorylation status of the protein tau, which is a neuronal cytoskeletal stabilizer. Conclusions/Significance These findings directly link free radicals of specific mitochondrial origin to AD-associated vascular and neuronal pathology. PMID:20479943

  12. Mitochondrial superoxide contributes to blood flow and axonal transport deficits in the Tg2576 mouse model of Alzheimer's disease.

    Directory of Open Access Journals (Sweden)

    Cynthia A Massaad

    Full Text Available BACKGROUND: Alzheimer's disease (AD is a neurodegenerative disease characterized by the progressive decline in cognitive functions and the deposition of aggregated amyloid beta (Abeta into senile plaques and the protein tau into tangles. In addition, a general state of oxidation has long been known to be a major hallmark of the disease. What is not known however, are the mechanisms by which oxidative stress contributes to the pathology of AD. METHODOLOGY/PRINCIPAL FINDINGS: In the current study, we used a mouse model of AD and genetically boosted its ability to quench free radicals of specific mitochondrial origin. We found that such manipulation conferred to the AD mice protection against vascular as well as neuronal deficits that typically affect them. We also found that the vascular deficits are improved via antioxidant modulation of the endothelial nitric oxide synthase, an enzyme primarily responsible for the production of nitric oxide, while neuronal deficits are improved via modulation of the phosphorylation status of the protein tau, which is a neuronal cytoskeletal stabilizer. CONCLUSIONS/SIGNIFICANCE: These findings directly link free radicals of specific mitochondrial origin to AD-associated vascular and neuronal pathology.

  13. Neuroanatomical and Neurochemical Basis of Impulsivity

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    Kemal Yazici

    2010-08-01

    tis paradigm, the tendency to prefer small immediate rewards over larger, more delayed reinforcers is measured. İmpulsive choice is defined by a greater tendency to value or choose smaller, more immediate reinforcers. Impulsivity is a multi-faceted behaviour. This behaviour may be studied by subdividing it into different processes neuroanatomically and neurochemically. Neuroanatomical data support the suggestion that behavioral disinhibition (impulsive action / motoric impulsivity and delay-discounting (impulsive choice / decision making differ in the degree to which various components of frontostriatal loops are implicated in their regulation. The dorsal prefrontal cortex does not appear to be involved in mediating impulsive choice, yet does have some role in regulating inhibitory processes. In contrast, there appears to be a pronounced role for the orbitofrontal cortex and basolateral amygdala in controlling impulsive choice. Other structures, however, such as the nucleus accumbens and subthalamic nucleus may be common to both circuits. From the neurochemical perspective, dopamine system and dopamine- 2 (D2 receptors in particular, seems to be closely involved in making impulsive choice. When the noradrenaline system does not function optimally, it might contribute to increased impulsivity. Serotonin might act upon prefrontal cortex to decrease impulsive choices. Interactions between the serotonin and the dopamine systems are important in the regulation of impulsive behaviour. It is possible that various receptor subtypes of the serotonin system may exert differing and even contrasting effects on impulsive behaviour. Although it is very informative to study neurotransmitter systems separately, it should be kept in mind that there are very intimate interactions between the neurotransmitter systems mentioned above. Based on the fact that impulsivity is regulated through multiple neurotransmitters and even more receptors, one may suggest that pharmacotherapy of

  14. Interactive Contributions of Cumulative Peer Stress and Executive Function Deficits to Depression in Early Adolescence

    Science.gov (United States)

    Agoston, Anna M.; Rudolph, Karen D.

    2016-01-01

    Exposure to peer stress contributes to adolescent depression, yet not all youth experience these effects. Thus, it is important to identify individual differences that shape the consequences of peer stress. This research investigated the interactive contribution of cumulative peer stress during childhood (second-fifth grades) and executive…

  15. The Brazilian contribution to Attention-Deficit/Hyperactivity Disorder molecular genetics in children and adolescents

    Science.gov (United States)

    Genro, Júlia Pasqualini; Roman, Tatiana; Rohde, Luis Augusto; Hutz, Mara Helena

    2012-01-01

    Attention-Deficit/Hyperactivity Disorder (ADHD) is a common psychiatric condition of children worldwide. This disorder is defined by a combination of symptoms of inattention and hyperactivity/impulsivity. Diagnosis is based on a sufficient number of symptoms causing impairment in these two domains determining several problems in personal and academic life. Although genetic and environmental factors are important in ADHD etiology, how these factors influence the brain and consequently behavior is still under debate. It seems to be consensus that a frontosubcortical dysfunction is responsible, at least in part, for the ADHD phenotype spectrum. The main results from association and pharmacogenetic studies performed in Brazil are discussed. The investigations performed so far on ADHD genetics in Brazil and elsewhere are far from conclusive. New plausible biological hypotheses linked to neurotransmission and neurodevelopment, as well as new analytic approaches are needed to fully disclose the genetic component of the disorder. PMID:23411749

  16. Pyk2 modulates hippocampal excitatory synapses and contributes to cognitive deficits in a Huntington’s disease model

    KAUST Repository

    Giralt, Albert

    2017-05-30

    The structure and function of spines and excitatory synapses are under the dynamic control of multiple signalling networks. Although tyrosine phosphorylation is involved, its regulation and importance are not well understood. Here we study the role of Pyk2, a non-receptor calcium-dependent protein-tyrosine kinase highly expressed in the hippocampus. Hippocampal-related learning and CA1 long-term potentiation are severely impaired in Pyk2-deficient mice and are associated with alterations in NMDA receptors, PSD-95 and dendritic spines. In cultured hippocampal neurons, Pyk2 has autophosphorylation-dependent and -independent roles in determining PSD-95 enrichment and spines density. Pyk2 levels are decreased in the hippocampus of individuals with Huntington and in the R6/1 mouse model of the disease. Normalizing Pyk2 levels in the hippocampus of R6/1 mice rescues memory deficits, spines pathology and PSD-95 localization. Our results reveal a role for Pyk2 in spine structure and synaptic function, and suggest that its deficit contributes to Huntington’s disease cognitive impairments.

  17. Social behaviour following severe traumatic brain injury: contribution of emotion perception deficits.

    Science.gov (United States)

    Saxton, Melissa E; Younan, Shameran Slewa; Lah, Suncica

    2013-01-01

    This theoretically driven study aimed to determine contribution of emotional perception impairments to social behaviour following traumatic brain injury (TBI). Adults with severe TBI (n = 24) participated. Emotion perception predictors included: (i) appraisal: Montreal Set of Facial Displays of Emotion, The Adapted Story Task, (ii) affective state: Depression, Anxiety and Stress Scale (DASS-21), Interpersonal Reactivity Index (IRI) and (iii) regulation: Delis Kaplan Executive Function System - Colour Word Interference and Word Fluency. Social behavioural outcomes were (i) interpersonal: Key Behaviors Change Inventory (KBCI) - Interpersonal Difficulties and (ii) communication: KBCI - Communication Problems. Social behaviours correlated with affective state, but not appraisal or regulation. Simultaneous regression analyses revealed significant independent contributions of affective state: (i) the IRI Perspective Taking to the KBCI Interpersonal Difficulties and (ii) the DASS-21 (composite) and IRI Perspective Taking to the KBCI Communication Problems. The models explained 52% and 72% of the variance of the KBCI Interpersonal Difficulties and Communication Problems respectively. This study provides evidence that impairments in certain aspects of emotion perception: affective state [empathy (perspective taking) and mood], but not appraisal and regulation, contribute to social behaviour difficulties in patients with severe TBI, which has important implications for rehabilitation.

  18. Neurochemical measurements in the zebrafish brain

    Directory of Open Access Journals (Sweden)

    Lauren eJones

    2015-09-01

    Full Text Available The zebrafish is an ideal model organism for behavioural genetics and neuroscience. The high conservation of genes and neurotransmitter pathways between zebrafish and other vertebrates permits the translation of research between species. Zebrafish behaviour can be studied at both larval and adult stages and recent research has begun to establish zebrafish models for human disease. Fast scan cyclic voltammetry (FSCV is an electrochemical technique that permits the detection of neurotransmitter release and reuptake. In this study we have used in vitro FSCV to measure the release of analytes in the adult zebrafish telencephalon. We compare different stimulation methods and present a characterisation of neurochemical changes in the wild-type zebrafish brain. This study represents the first FSCV recordings in zebrafish, thus paving the way for neurochemical analysis of the fish brain.

  19. Neurochemical measurements in the zebrafish brain

    Science.gov (United States)

    Jones, Lauren J.; McCutcheon, James E.; Young, Andrew M. J.; Norton, William H. J.

    2015-01-01

    The zebrafish is an ideal model organism for behavioral genetics and neuroscience. The high conservation of genes and neurotransmitter pathways between zebrafish and other vertebrates permits the translation of research between species. Zebrafish behavior can be studied at both larval and adult stages and recent research has begun to establish zebrafish models for human disease. Fast scan cyclic voltammetry (FSCV) is an electrochemical technique that permits the detection of neurotransmitter release and reuptake. In this study we have used in vitro FSCV to measure the release of analytes in the adult zebrafish telencephalon. We compare different stimulation methods and present a characterization of neurochemical changes in the wild-type zebrafish brain. This study represents the first FSCV recordings in zebrafish, thus paving the way for neurochemical analysis of the fish brain. PMID:26441575

  20. SOME NEUROCHEMICAL DISTURBANCES IN MULTIPLE SCLEROSIS

    OpenAIRE

    Vladimir V. Markelov; Maxim V. Trushin

    2006-01-01

    ABSTRACTThe data presented in this manuscript suggest a pivotal role of the central nervous system (CNS) in the regulation of immune status. We describe here that some neurochemical disturbances may provoke development of various diseases including multiple sclerosis. Some theoretic and practical backgrounds, how to improve the multiple sclerosis sufferers and patients with other autoimmune disorders, are also given.RESUMENLos datos que presentamos en este manuscrito, sugieren un papel guia d...

  1. Neurochemical alterations associated with borderline personality disorder.

    Science.gov (United States)

    Atmaca, Murad; Karakoc, Tevfik; Mermi, Osman; Gurkan Gurok, M; Yildirim, Hanefi

    2015-01-01

    In neuroimaging on borderline personality disorder, prior studies focused on the hippocampus and amygdala, as mentioned above. However, no study investigated whether there were neurochemical changes in the patients with borderline personality disorder. Therefore, in the present study, we aimed to investigate neurochemical change of patients diagnosed with borderline disorder and hypothesized that neurochemicals would change in the hippocampus region of these patients. Seventeen patients and the same number of healthy control subjects were analyzed by using a 1.5 Tesla GE Signa Imaging System. N-acetylaspartate (NAA), choline compounds (CHO), and creatine (CRE) values of hippocampal region were measured. The mean NAA/CRE ratio in the hippocampus region was significantly reduced in the patients with borderline personality disorder compared to that of healthy control subjects, In addition, NAA/CHO ratio of the patients with borderline personality disorder was also significantly reduced when compared to that of healthy subjects. There was no difference in the ratio of CHO/CRE. In summary, we present evidence for reduced NAA in the patients with borderline personality disorder. © 2015, The Author(s).

  2. Vanillin Attenuated Behavioural Impairments, Neurochemical Deficts, Oxidative Stress and Apoptosis Against Rotenone Induced Rat Model of Parkinson's Disease.

    Science.gov (United States)

    Dhanalakshmi, Chinnasamy; Janakiraman, Udaiyappan; Manivasagam, Thamilarasan; Justin Thenmozhi, Arokiasamy; Essa, Musthafa Mohamed; Kalandar, Ameer; Khan, Mohammed Abdul Sattar; Guillemin, Gilles J

    2016-08-01

    Vanillin (4-hydroxy-3-methoxybenzaldehyde), a pleasant smelling organic aromatic compound, is widely used as a flavoring additive in food, beverage, cosmetic and drug industries. It is reported to cross the blood brain barrier and also displayed antioxidant and neuroprotective activities. We previously reported the neuroprotective effect of vanillin against rotenone induced in in vitro model of PD. The present experiment was aimed to analyze the neuroprotective effect of vanillin on the motor and non-motor deficits, neurochemical variables, oxidative, anti-oxidative indices and the expression of apoptotic markers against rotenone induced rat model of Parkinson's disease (PD). Rotenone treatment exhibited motor and non-motor impairments, neurochemical deficits, oxidative stress and apoptosis, whereas oral administration of vanillin attenuated the above-said indices. However further studies are needed to explore the mitochondrial protective and anti-inflammatory properties of vanillin, as these processes play a vital role in the cause and progression of PD.

  3. Behavioral metabolomics analysis identifies novel neurochemical signatures in methamphetamine sensitization

    OpenAIRE

    Adkins, Daniel E.; McClay, Joseph L.; VUNCK, SARAH A.; Batman, Angela M.; Vann, Robert E.; Clark, Shaunna L.; SOUZA,RENAN P. DE; Crowley, James J.; Sullivan, Patrick F; van den Oord, Edwin J.C.G.; Beardsley, Patrick M.

    2013-01-01

    Behavioral sensitization has been widely studied in animal models and is theorized to reflect neural modifications associated with human psychostimulant addiction. While the mesolimbic dopaminergic pathway is known to play a role, the neurochemical mechanisms underlying behavioral sensitization remain incompletely understood. In the present study, we conducted the first metabolomics analysis to globally characterize neurochemical differences associated with behavioral sensitization. Methamphe...

  4. SOME NEUROCHEMICAL DISTURBANCES IN MULTIPLE SCLEROSIS

    Directory of Open Access Journals (Sweden)

    Vladimir V. Markelov

    2006-04-01

    Full Text Available ABSTRACTThe data presented in this manuscript suggest a pivotal role of the central nervous system (CNS in the regulation of immune status. We describe here that some neurochemical disturbances may provoke development of various diseases including multiple sclerosis. Some theoretic and practical backgrounds, how to improve the multiple sclerosis sufferers and patients with other autoimmune disorders, are also given.RESUMENLos datos que presentamos en este manuscrito, sugieren un papel guia del sistema nervioso central (SNC en la regulación del estado inmune. Describimos aquí que varias alteraciones neuroquímicas pueden provocar el desarrollo de varias enfermedades, incluyendo esclerosis múltiple. También se comenta acerca del trasfondo teórico y práctico, y cómo mejorar a víctimas y pacientes con esclerosis múltiple y otras alteraciones autoinmunes.

  5. Deficits in the activity of presynaptic γ-aminobutyric acid type B receptors contribute to altered neuronal excitability in fragile X syndrome.

    Science.gov (United States)

    Kang, Ji-Yong; Chadchankar, Jayashree; Vien, Thuy N; Mighdoll, Michelle I; Hyde, Thomas M; Mather, Robert J; Deeb, Tarek Z; Pangalos, Menelas N; Brandon, Nicholas J; Dunlop, John; Moss, Stephen J

    2017-04-21

    The behavioral and anatomical deficits seen in fragile X syndrome (FXS) are widely believed to result from imbalances in the relative strengths of excitatory and inhibitory neurotransmission. Although modified neuronal excitability is thought to be of significance, the contribution that alterations in GABAergic inhibition play in the pathophysiology of FXS are ill defined. Slow sustained neuronal inhibition is mediated by γ-aminobutyric acid type B (GABA B ) receptors, which are heterodimeric G-protein-coupled receptors constructed from R1a and R2 or R1b and R2 subunits. Via the activation of G i/o , they limit cAMP accumulation, diminish neurotransmitter release, and induce neuronal hyperpolarization. Here we reveal that selective deficits in R1a subunit expression are seen in Fmr1 knock-out mice (KO) mice, a widely used animal model of FXS, but the levels of the respective mRNAs were unaffected. Similar trends of R1a expression were seen in a subset of FXS patients. GABA B receptors (GABA B Rs) exert powerful pre- and postsynaptic inhibitory effects on neurotransmission. R1a-containing GABA B Rs are believed to mediate presynaptic inhibition in principal neurons. In accordance with this result, deficits in the ability of GABA B Rs to suppress glutamate release were seen in Fmr1-KO mice. In contrast, the ability of GABA B Rs to suppress GABA release and induce postsynaptic hyperpolarization was unaffected. Significantly, this deficit contributes to the pathophysiology of FXS as the GABA B R agonist ( R )-baclofen rescued the imbalances between excitatory and inhibitory neurotransmission evident in Fmr1-KO mice. Collectively, our results provided evidence that selective deficits in the activity of presynaptic GABA B Rs contribute to the pathophysiology of FXS. © 2017 by The American Society for Biochemistry and Molecular Biology, Inc.

  6. Addiction is a reward deficit and stress surfeit disorder

    Directory of Open Access Journals (Sweden)

    George F Koob

    2013-08-01

    Full Text Available Drug addiction can be defined by a three-stage cycle—binge/intoxication, withdrawal/negative affect, and preoccupation/anticipation—that involves allostatic changes in the brain reward and stress systems. Two primary sources of reinforcement, positive and negative reinforcement, have been hypothesized to play a role in this allostatic process. The negative emotional state that drives negative reinforcement is hypothesized to derive from dysregulation of key neurochemical elements involved in the brain reward and stress systems. Specific neurochemical elements in these structures include not only decreases in reward system function (within-system opponent processes but also recruitment of the brain stress systems mediated by corticotropin-releasing factor (CRF and dynorphin-κ opioid systems in the ventral striatum, extended amygdala, and frontal cortex (both between-system opponent processes. CRF antagonists block anxiety-like responses associated with withdrawal, block increases in reward thresholds produced by withdrawal from drugs of abuse, and block compulsive-like drug taking during extended access. Excessive drug taking also engages the activation of CRF in the medial prefrontal cortex, paralleled by deficits in executive function that may facilitate the transition to compulsive-like responding. Neuropeptide Y, a powerful anti-stress neurotransmitter, has a profile of action on compulsive-like responding for ethanol similar to a CRF1 antagonist. Blockade of the κ opioid system can also block dysphoric-like effects associated with withdrawal from drugs of abuse and block the development of compulsive-like responding during extended access to drugs of abuse, suggesting another powerful brain stress system that contributes to compulsive drug seeking. The loss of reward function and recruitment of brain systems provide a powerful neurochemical basis that drives the compulsivity of addiction.

  7. Autism and Fragile X: Is There a Neurochemical Link?

    Directory of Open Access Journals (Sweden)

    Nagwa A. Meguid

    2014-12-01

    CONCLUSIONS: Autism and Fragile X syndrome share some neurochemical similarities with regards of high Glutamate and GABA levels while Serotonin was significantly different in the 2 disorders and may be used a unique biomarker for autism.

  8. Leaf developmental stage modulates metabolite accumulation and photosynthesis contributing to acclimation of Arabidopsis thaliana to water deficit.

    Science.gov (United States)

    Sperdouli, Ilektra; Moustakas, Michael

    2014-07-01

    We examined whether young and mature leaves of Arabidopsis thaliana in their response to mild water deficit (MiWD) and moderate water deficit (MoWD), behave differentially, and whether photosynthetic acclimation to water deficit correlates with increased proline and sugar accumulation. We observed that with increasing water deficit, leaf relative water content decreased, while proline and sugar accumulation increased in both leaf-developmental stages. Under both MiWD and MoWD, young leaves showed less water loss and accumulated higher level of metabolites compared to mature leaves. This, leaf age-related increase in metabolite accumulation that was significantly higher under MoWD, allowed young leaves to cope with oxidative damage by maintaining their base levels of lipid peroxidation. Thus, acclimation of young leaves to MoWD, involves a better homeostasis of reactive oxygen species (ROS), that was achieved among others by (1) increased sugar accumulation and (2) either increased proline synthesis and/or decreased proline catabolism, that decrease the NADPH/NADP(+) ratio, resulting in a higher level of oxidized state of quinone A and thus in a reduced excitation pressure, and by (3) stimulation of the photoprotective mechanism of non-photochemical quenching, that reflects the dissipation of excess excitation energy in the form of harmless heat, thus protecting the plant from the damaging effects of ROS.

  9. Peer Rejection and Friendships in Children with Attention-Deficit/Hyperactivity Disorder: Contributions to Long-Term Outcomes

    Science.gov (United States)

    Mrug, Sylvie; Molina, Brooke S. G.; Hoza, Betsy; Gerdes, Alyson C.; Hinshaw, Stephen P.; Hechtman, Lily; Arnold, L. Eugene

    2012-01-01

    Even after evidence-based treatment, Attention-Deficit/Hyperactivity Disorder (ADHD) is associated with poor long-term outcomes. These outcomes may be partly explained by difficulties in peer functioning, which are common among children with ADHD and which do not respond optimally to standard ADHD treatments. We examined whether peer rejection and…

  10. Deficits in auditory processing contribute to impairments in vocal affect recognition in autism spectrum disorders: A MEG study.

    Science.gov (United States)

    Demopoulos, Carly; Hopkins, Joyce; Kopald, Brandon E; Paulson, Kim; Doyle, Lauren; Andrews, Whitney E; Lewine, Jeffrey David

    2015-11-01

    The primary aim of this study was to examine whether there is an association between magnetoencephalography-based (MEG) indices of basic cortical auditory processing and vocal affect recognition (VAR) ability in individuals with autism spectrum disorder (ASD). MEG data were collected from 25 children/adolescents with ASD and 12 control participants using a paired-tone paradigm to measure quality of auditory physiology, sensory gating, and rapid auditory processing. Group differences were examined in auditory processing and vocal affect recognition ability. The relationship between differences in auditory processing and vocal affect recognition deficits was examined in the ASD group. Replicating prior studies, participants with ASD showed longer M1n latencies and impaired rapid processing compared with control participants. These variables were significantly related to VAR, with the linear combination of auditory processing variables accounting for approximately 30% of the variability after controlling for age and language skills in participants with ASD. VAR deficits in ASD are typically interpreted as part of a core, higher order dysfunction of the "social brain"; however, these results suggest they also may reflect basic deficits in auditory processing that compromise the extraction of socially relevant cues from the auditory environment. As such, they also suggest that therapeutic targeting of sensory dysfunction in ASD may have additional positive implications for other functional deficits. (c) 2015 APA, all rights reserved).

  11. Central Neurochemical Ultradian Variability in Depression

    Directory of Open Access Journals (Sweden)

    Ronald M. Salomon

    2006-01-01

    Full Text Available Depression is characterized by blunted behavior and neuroendocrine function that generally improve with antidepressant treatment. This study examined intrinsic variability in brain neurotransmitter function, since it may be a source of blunted behavior and neuroendocrine function in depression and a marker for the illness, and has not previously been analyzed using wavelet decomposition. To measure variability in monoamine metabolites, lumbar cerebrospinal fluid (CSF was collected in serial samples in depressed patients before and after treatment. We hypothesized that changes in variability would be observed after treatment. Mechanisms that control such variability may be critical to the pathophysiology of depression. Method: Time series data was obtained from serial ten-min sampling over a 24-hr period (N = 144 from thirteen depressed patients, with a repeat collection after 5 weeks of antidepressant (sertraline or bupropion treatment. Concentrations of tryptophan (TRP, the monoamine metabolites 5-HIAA (metabolite of serotonin and HVA (metabolite of dopamine, and the HVA:5HIAA ratio were transformed to examine power in slowly (160 min/cycle to rapidly (20 min/cycle occurring events. Power, the sum of the squares of the coefficients in each d (detail wavelet, reflects variability within a limited frequency bandwidth for that wavelet. Pre-treatment to post-treatment comparisons were conducted with repeated measures ANOVA. Results: Antidepressant treatment was associated with increased power in the d2 wavelet from the HVA (p = 0.03 and the HVA:5-HIAA ratio (p = 0.03 series. The d1 and d3 wavelets showed increased power following antidepressant treatment for the ratio series (d1, p = 0.01; d3, p = 0.05. Significant changes in power were not observed for the 5-HIAA data series. Power differences among analytes suggest that the findings are specific to each system. Conclusion: The wavelet transform analysis shows changes in neurochemical signal

  12. Visual processing in reading disorders and attention-deficit/hyperactivity disorder and its contribution to basic reading ability

    Directory of Open Access Journals (Sweden)

    Michelle Y. Kibby

    2015-10-01

    Full Text Available Whether visual processing deficits are common in reading disorders (RD, and related to reading ability in general, has been debated for decades. The type of visual processing affected also is debated, although visual discrimination and short-term memory (STM may be more commonly related to reading ability. Reading disorders are frequently comorbid with ADHD, and children with ADHD often have subclinical reading problems. Hence, children with ADHD were used as a comparison group in this study. ADHD and RD may be dissociated in terms of visual processing. Whereas RD may be associated with deficits in visual discrimination and short-term memory for order, ADHD is associated with deficits in visual-spatial processing. Thus, we hypothesized that children with RD would perform worse than controls and children with ADHD only on a measure of visual discrimination and a measure of visual STM that requires memory for order. We expected all groups would perform comparably on the measure of visual STM that does not require sequential processing. We found children with RD or ADHD were commensurate to controls on measures of visual discrimination and visual STM that do not require sequential processing. In contrast, both RD groups (RD, RD/ADHD performed worse than controls on the measure of visual STM that requires memory for order, and children with comorbid RD/ADHD performed worse than those with ADHD. In addition, of the three visual measures, only sequential visual STM predicted reading ability. Hence, our findings suggest there is a deficit in visual sequential STM that is specific to RD and is related to basic reading ability. The source of this deficit is worthy of further research, but it may include both reduced memory for order and poorer verbal mediation.

  13. Contribution of different regions of the prefrontal cortex and lesion laterality to deficit of decision-making on the Iowa Gambling Task.

    Science.gov (United States)

    Ouerchefani, Riadh; Ouerchefani, Naoufel; Allain, Philippe; Ben Rejeb, Mohamed Riadh; Le Gall, Didier

    2017-02-01

    Few studies have examined the contribution of different sub-regions of the prefrontal cortex and lesion laterality to decision-making abilities. In addition, there are inconsistent findings about the role of ventromedial and dorsolateral lesions in decision-making deficit. In this study, decision-making processes are investigated following different damaged areas of the prefrontal cortex. We paid particular attention to the contribution of laterality, lesion location and lesion volume in decision-making deficit. Twenty-seven patients with discrete ventromedial lesions, dorsolateral lesions or extended-frontal lesions were compared with normal subjects on the Iowa Gambling Task (IGT). Our results showed that all frontal subgroups were impaired on the IGT in comparison with normal subjects. We noted also that IGT performance did not vary systematically based on lesion laterality or location. More precisely, our lesion analysis revealed that decision-making processes depend on a large cerebral network, including both ventromedial and dorsolateral areas of the prefrontal cortex. Consistent with past findings, our results support the claim that IGT deficit is not solitarily associated with ventromedial prefrontal cortex lesions. Copyright © 2016 Elsevier Inc. All rights reserved.

  14. Neurochemical dynamics of acute orofacial pain in the human trigeminal brainstem nuclear complex.

    Science.gov (United States)

    de Matos, Nuno M P; Hock, Andreas; Wyss, Michael; Ettlin, Dominik A; Brügger, Mike

    2017-09-04

    The trigeminal brainstem sensory nuclear complex is the first central relay structure mediating orofacial somatosensory and nociceptive perception. Animal studies suggest a substantial involvement of neurochemical alterations at such basal CNS levels in acute and chronic pain processing. Translating this animal based knowledge to humans is challenging. Human related examining of brainstem functions are challenged by MR related peculiarities as well as applicability aspects of experimentally standardized paradigms. Based on our experience with an MR compatible human orofacial pain model, the aims of the present study were twofold: 1) from a technical perspective, the evaluation of proton magnetic resonance spectroscopy at 3 T regarding measurement accuracy of neurochemical profiles in this small brainstem nuclear complex and 2) the examination of possible neurochemical alterations induced by an experimental orofacial pain model. Data from 13 healthy volunteers aged 19-46 years were analyzed and revealed high quality spectra with significant reductions in total N-acetylaspartate (N-acetylaspartate + N-acetylaspartylglutamate) (-3.7%, p = 0.009) and GABA (-10.88%, p = 0.041) during the pain condition. These results might reflect contributions of N-acetylaspartate and N-acetylaspartylglutamate in neuronal activity-dependent physiologic processes and/or excitatory neurotransmission, whereas changes in GABA might indicate towards a reduction in tonic GABAergic functioning during nociceptive signaling. Summarized, the present study indicates the applicability of (1)H-MRS to obtain neurochemical dynamics within the human trigeminal brainstem sensory nuclear complex. Further developments are needed to pave the way towards bridging important animal based knowledge with human research to understand the neurochemistry of orofacial nociception and pain. Copyright © 2017 Elsevier Inc. All rights reserved.

  15. Neurochemical mechanisms underlying responses to psychostimulants

    Energy Technology Data Exchange (ETDEWEB)

    Volkow, N.D.; Fowler, J.S.; Hitzemann, R.; Wang, G.J. [Brookhaven National Lab., Upton, NY (United States)]|[State Univ. of New York, Stony Brook, NY (United States)

    1994-11-01

    This study employed positron emission tomography (PET) to investigate biochemical and metabolic characteristics of the brain of individuals which could put them at risk for drug addiction. It takes advantage of the normal variability between individuals in response to psychoactive drugs to investigate relation between mental state, brain neurochemistry and metabolism and the behavioral response to drugs. We discuss its use to assess if there is an association between mental state and dompaminergic reactivity in response to the psychostimulant drug methylphenidate (MP). Changes in synaptic dopamine induced by MP were evaluated with PET and [11C]raclopride, a D{sub 2} receptor radioligand that is sensitive to endogenous dopamine. Methylpphenidate significantly decreased striatal [11C]raclopride binding. The study showed a correlation between the magnitude of the dopamine-induced changes by methylphenidate, and the mental state of the subjects. Subjects reporting high levels of anxiety and restlessness at baseline had larger changes in MP-induced dopamine changes than those that did not. Further investigations on the relation between an individual`s response to a drug and his/her mental state and personality as well as his neurochemical brain composition may enable to understand better differences in drug addiction vulnerability.

  16. Carbon Nanofiber Electrode Array for Neurochemical Monitoring

    Science.gov (United States)

    Koehne, Jessica E.

    2017-01-01

    A sensor platform based on vertically aligned carbon nanofibers (CNFs) has been developed. Their inherent nanometer scale, high conductivity, wide potential window, good biocompatibility and well-defined surface chemistry make them ideal candidates as biosensor electrodes. Here, we report using vertically aligned CNF as neurotransmitter recording electrodes for application in a smart deep brain stimulation (DBS) device. Our approach combines a multiplexed CNF electrode chip, developed at NASA Ames Research Center, with the Wireless Instantaneous Neurotransmitter Concentration Sensor (WINCS) system, developed at the Mayo Clinic. Preliminary results indicate that the CNF nanoelectrode arrays are easily integrated with WINCS for neurotransmitter detection in a multiplexed array format. In the future, combining CNF based stimulating and recording electrodes with WINCS may lay the foundation for an implantable smart therapeutic system that utilizes neurochemical feedback control while likely resulting in increased DBS application in various neuropsychiatric disorders. In total, our goal is to take advantage of the nanostructure of CNF arrays for biosensing studies requiring ultrahigh sensitivity, high-degree of miniaturization, and selective biofunctionalization.

  17. Elevated progranulin contributes to synaptic and learning deficit due to loss of fragile X mental retardation protein.

    Science.gov (United States)

    Zhang, Kun; Li, Yu-Jiao; Guo, Yanyan; Zheng, Kai-Yin; Yang, Qi; Yang, Le; Wang, Xin-Shang; Song, Qian; Chen, Tao; Zhuo, Min; Zhao, Ming-Gao

    2017-12-01

    Fragile X syndrome is an inheritable form of intellectual disability caused by loss of fragile X mental retardation protein (FMRP, encoded by the FMR1 gene). Absence of FMRP caused overexpression of progranulin (PGRN, encoded by GRN), a putative tumour necrosis factor receptor ligand. In the present study, we found that progranulin mRNA and protein were upregulated in the medial prefrontal cortex of Fmr1 knock-out mice. In Fmr1 knock-out mice, elevated progranulin caused insufficient dendritic spine pruning and late-phase long-term potentiation in the medial prefrontal cortex of Fmr1 knock-out mice. Partial progranulin knock-down restored spine morphology and reversed behavioural deficits, including impaired fear memory, hyperactivity, and motor inflexibility in Fmr1 knock-out mice. Progranulin increased levels of phosphorylated glutamate ionotropic receptor GluA1 and nuclear factor kappa B in cultured wild-type neurons. Tumour necrosis factor receptor 2 antibody perfusion blocked the effects of progranulin on GluA1 phosphorylation; this result indicates that tumour necrosis factor receptor 2 is required for progranulin-mediated GluA1 phosphorylation and late-phase long-term potentiation expression. However, high basal level of progranulin in Fmr1 knock-out mice prevented further facilitation of synaptic plasticity by exogenous progranulin. Partial downregulation of progranulin or tumour necrosis factor receptor 2/nuclear factor kappa B signalling restored synaptic plasticity and memory deficits in Fmr1 knock-out mice. These findings suggest that elevated PGRN is linked to cognitive deficits of fragile X syndrome, and the progranulin/tumour necrosis factor receptor 2 signalling pathway may be a putative therapeutic target for improving cognitive deficits in fragile X syndrome. © The Author (2017). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.com.

  18. Differential contribution of APP metabolites to early cognitive deficits in a TgCRND8 mouse model of Alzheimer's disease.

    Science.gov (United States)

    Hamm, Valentine; Héraud, Céline; Bott, Jean-Bastien; Herbeaux, Karine; Strittmatter, Carole; Mathis, Chantal; Goutagny, Romain

    2017-02-01

    Alzheimer's disease (AD) is a neurodegenerative pathology commonly characterized by a progressive and irreversible deterioration of cognitive functions, especially memory. Although the etiology of AD remains unknown, a consensus has emerged on the amyloid hypothesis, which posits that increased production of soluble amyloid β (Aβ) peptide induces neuronal network dysfunctions and cognitive deficits. However, the relative failures of Aβ-centric therapeutics suggest that the amyloid hypothesis is incomplete and/or that the treatments were given too late in the course of AD, when neuronal damages were already too extensive. Hence, it is striking to see that very few studies have extensively characterized, from anatomy to behavior, the alterations associated with pre-amyloid stages in mouse models of AD amyloid pathology. To fulfill this gap, we examined memory capacities as well as hippocampal network anatomy and dynamics in young adult pre-plaque TgCRND8 mice when hippocampal Aβ levels are still low. We showed that TgCRND8 mice present alterations in hippocampal inhibitory networks and γ oscillations at this stage. Further, these mice exhibited deficits only in a subset of hippocampal-dependent memory tasks, which are all affected at later stages. Last, using a pharmacological approach, we showed that some of these early memory deficits were Aβ-independent. Our results could partly explain the limited efficacy of Aβ-directed treatments and favor multitherapy approaches for early symptomatic treatment for AD.

  19. Early life stress induces attention-deficit hyperactivity disorder (ADHD)-like behavioral and brain metabolic dysfunctions: functional imaging of methylphenidate treatment in a novel rodent model.

    Science.gov (United States)

    Bock, J; Breuer, S; Poeggel, G; Braun, K

    2017-03-01

    In a novel animal model Octodon degus we tested the hypothesis that, in addition to genetic predisposition, early life stress (ELS) contributes to the etiology of attention-deficit hyperactivity disorder-like behavioral symptoms and the associated brain functional deficits. Since previous neurochemical observations revealed that early life stress impairs dopaminergic functions, we predicted that these symptoms can be normalized by treatment with methylphenidate. In line with our hypothesis, the behavioral analysis revealed that repeated ELS induced locomotor hyperactivity and reduced attention towards an emotionally relevant acoustic stimulus. Functional imaging using ( 14 C)-2-fluoro-deoxyglucose-autoradiography revealed that the behavioral symptoms are paralleled by metabolic hypoactivity of prefrontal, mesolimbic and subcortical brain areas. Finally, the pharmacological intervention provided further evidence that the behavioral and metabolic dysfunctions are due to impaired dopaminergic neurotransmission. Elevating dopamine in ELS animals by methylphenidate normalized locomotor hyperactivity and attention-deficit and ameliorated brain metabolic hypoactivity in a dose-dependent manner.

  20. Diagnosing Contributions of Sensory and Cognitive Deficits to Hearing Dysfunction in Blast-Exposed/TBI Service Members

    Science.gov (United States)

    2017-10-01

    Kimberly Jenkins began actively recruiting potential study candidates during VA Compensation and Pension evaluations she conducts at the Zybs Medical...Research Identifier: 0000-0002-5096-5914 Nearest person month worked: 1 Contribution to project: Funding support: 9 Name: Dr. Kenneth Grant...Project Role: Co-Principal Investigator Research Identifier: Nearest person month worked: 1 Contribution to project: Funding support: Name: Scott

  1. Local-Global Visual Deficits in Williams Syndrome: Stimulus presence contributes to diminished performance on image-reproduction

    Directory of Open Access Journals (Sweden)

    Ana Maria Abreu

    2006-12-01

    Full Text Available Impairments in visuospatial processing exhibited by individuals with Williams Syndrome (WS have been ascribed to a local processing bias. The imprecise specification of this local bias hypothesis has led to contradictions between different accounts of the visuospatial deficits in WS. We present two experiments investigating visual processing of geometric Navon stimuli by children with WS. The first experiment examined image reproduction in a visuoconstruction task and the second experiment explored the effect of manipulating global salience on recognition of visual stimuli by varying the density of local elements possessed by the stimuli. In the visuoconstruction task, the children with WS did show a local bias with respect to controls, but only when the target being copied was present; when drawing from memory, subjects with WS produced a heterogeneous pattern of answers. In the recognition task, children with WS exhibited the same sensitivity to global figures as matched controls, confirming previous findings in which no local bias in perception was found in WS subjects. We propose that subjects with WS are unable to disengage their attention from local elements during the planning stage of image reproduction (a visual-conflict hypothesis.

  2. Nitric oxide contributes to learning and memory deficits observed in hypothyroid rats during neonatal and juvenile growth

    Directory of Open Access Journals (Sweden)

    Mahmoud Hosseini

    2010-01-01

    Full Text Available INTRODUCTION: Severe cognitive impairment follows thyroid hormone deficiency during the neonatal period. The role of nitric oxide (NO in learning and memory has been widely investigated. METHODS: This study aimed to investigate the effect of hypothyroidism during neonatal and juvenile periods on NO metabolites in the hippocampi of rats and on learning and memory. Animals were divided into two groups and treated for 60 days from the first day of lactation. The control group received regular water, whereas animals in a separate group were given water supplemented with 0.03% methimazole to induce hypothyroidism. Male offspring were selected and tested in the Morris water maze. Samples of blood were collected to measure the metabolites of NO, NO2, NO3 and thyroxine. The animals were then sacrificed, and their hippocampi were removed to measure the tissue concentrations of NO2 and NO3. DISCUSSION: Compared to the control group's offspring, serum thyroxine levels in the methimazole group's offspring were significantly lower (P<0.01. In addition, the swim distance and time latency were significantly higher in the methimazole group (P<0.001, and the time spent by this group in the target quadrant (Q1 during the probe trial was significantly lower (P<0.001. There was no significant difference in the plasma levels of NO metabolites between the two groups; however, significantly higher NO metabolite levels in the hippocampi of the methimazole group were observed compared to controls (P<0.05. CONCLUSION: These results suggest that the increased NO level in the hippocampus may play a role in the learning and memory deficits observed in childhood hypothyroidism; however, the precise underlying mechanism(s remains to be elucidated.

  3. Anandamide-CB1 receptor signaling contributes to postnatal ethanol-induced neonatal neurodegeneration, adult synaptic, and memory deficits.

    Science.gov (United States)

    Subbanna, Shivakumar; Shivakumar, Madhu; Psychoyos, Delphine; Xie, Shan; Basavarajappa, Balapal S

    2013-04-10

    The transient exposure of immature rodents to ethanol during postnatal day 7 (P7), which is comparable with the third trimester in human pregnancy, induces synaptic dysfunctions. However, the molecular mechanisms underlying these dysfunctions are still poorly understood. Although the endocannabinoid system has been shown to be an important modulator of ethanol sensitivity in adult mice, its potential role in synaptic dysfunctions in mice exposed to ethanol during early brain development is not examined. In this study, we investigated the potential role of endocannabinoids and the cannabinoid receptor type 1 (CB1R) in neonatal neurodegeneration and adult synaptic dysfunctions in mice exposed to ethanol at P7. Ethanol treatment at P7, which induces neurodegeneration, increased anandamide (AEA) but not 2-arachidonylglycerol biosynthesis and CB1R protein expression in the hippocampus and cortex, two brain areas that are important for memory formation and storage, respectively. N-Arachidonoyl phosphatidylethanolamine-phospholipase D (NAPE-PLD), glycerophosphodiesterase (GDE1), and CB1R protein expression were enhanced by transcriptional activation of the genes encoding NAPE-PLD, GDE1, and CB1R proteins, respectively. In addition, ethanol inhibited ERK1/2 and AKT phosphorylation. The blockade of CB1Rs before ethanol treatment at P7 relieved ERK1/2 but not AKT phosphorylation and prevented neurodegeneration. CB1R knock-out mice exhibited no ethanol-induced neurodegeneration and inhibition of ERK1/2 phosphorylation. The protective effects of CB1R blockade through pharmacological or genetic deletion resulted in normal adult synaptic plasticity and novel object recognition memory in mice exposed to ethanol at P7. The AEA/CB1R/pERK1/2 signaling pathway may be directly responsible for the synaptic and memory deficits associated with fetal alcohol spectrum disorders.

  4. Thalamic volume deficit contributes to procedural and explicit memory impairment in HIV infection with primary alcoholism comorbidity.

    Science.gov (United States)

    Fama, Rosemary; Rosenbloom, Margaret J; Sassoon, Stephanie A; Rohlfing, Torsten; Pfefferbaum, Adolf; Sullivan, Edith V

    2014-12-01

    Component cognitive and motor processes contributing to diminished visuomotor procedural learning in HIV infection with comorbid chronic alcoholism (HIV+ALC) include problems with attention and explicit memory processes. The neural correlates associated with this constellation of cognitive and motor processes in HIV infection and alcoholism have yet to be delineated. Frontostriatal regions are affected in HIV infection, frontothalamocerebellar regions are affected in chronic alcoholism, and frontolimbic regions are likely affected in both; all three of these systems have the potential of contributing to both visuomotor procedural learning and explicit memory processes. Here, we examined the neural correlates of implicit memory, explicit memory, attention, and motor tests in 26 HIV+ALC (5 with comorbidity for nonalcohol drug abuse/dependence) and 19 age-range matched healthy control men. Parcellated brain volumes, including cortical, subcortical, and allocortical regions, as well as cortical sulci and ventricles, were derived using the SRI24 brain atlas. Results indicated that smaller thalamic volumes were associated with poorer performance on tests of explicit (immediate and delayed) and implicit (visuomotor procedural) memory in HIV+ALC. By contrast, smaller hippocampal volumes were associated with lower scores on explicit, but not implicit memory. Multiple regression analyses revealed that volumes of both the thalamus and the hippocampus were each unique independent predictors of explicit memory scores. This study provides evidence of a dissociation between implicit and explicit memory tasks in HIV+ALC, with selective relationships observed between hippocampal volume and explicit but not implicit memory, and highlights the relevance of the thalamus to mnemonic processes.

  5. Curcumin ameliorates reserpine-induced pain-depression dyad: behavioural, biochemical, neurochemical and molecular evidences.

    Science.gov (United States)

    Arora, V; Kuhad, A; Tiwari, V; Chopra, K

    2011-11-01

    An apparent clinical relationship between pain and depression has long been recognized. Depression and pain are often diagnosed in the same patients. The emerging concept for pain-depression pathogenesis is the dysfunction of biogenic amine-mediated pain-depression control and the possible involvement of nitrodative stress-induced neurogenic inflammation. The present study was designed to investigate the effect of curcumin on reserpine-induced pain-depression dyad in rats. Administration of reserpine (1mg/kg subcutaneous daily for three consecutive days) led to a significant decrease in nociceptive threshold as evident from reduced paw withdrawal threshold in Randall Sellitto and von-Frey hair test as well as significant increase in immobility time in forced swim test. This behavioural deficit was integrated with decrease in the biogenic amine (dopamine, norepinephrine and serotonin) levels along with increased substance P concentration, nitrodative stress, inflammatory cytokines, NF-κβ and caspase-3 levels in different brain regions (cortex and hippocampus) of the reserpinised rats. Curcumin (100, 200, 300mg/kg; ip) dose dependently ameliorated the behavioural deficits associated with pain and depression by restoring behavioural, biochemical, neurochemical and molecular alterations against reserpine-induced pain-depression dyad in rats. Copyright © 2011 Elsevier Ltd. All rights reserved.

  6. Neurochemical organization of the nucleus paramedianus dorsalis in the human

    OpenAIRE

    Baizer, Joan S.; Baker, James F.; Haas, Kristin; Lima, Raquel

    2007-01-01

    We have characterized the neurochemical organization of a small brainstem nucleus in the human brain, the nucleus paramedianus dorsalis (PMD). PMD is located adjacent and medial to the nucleus prepositus hypoglossi (PH) in the dorsal medulla, and is distinguished by the pattern of immunoreactivity of cells and fibers to several markers including calcium-binding proteins, a synthetic enzyme for nitric oxide (neuronal nitric oxide synthase, nNOS) and a nonphosphorylated neurofilament protein (a...

  7. Behavioral metabolomics analysis identifies novel neurochemical signatures in methamphetamine sensitization.

    Science.gov (United States)

    Adkins, D E; McClay, J L; Vunck, S A; Batman, A M; Vann, R E; Clark, S L; Souza, R P; Crowley, J J; Sullivan, P F; van den Oord, E J C G; Beardsley, P M

    2013-11-01

    Behavioral sensitization has been widely studied in animal models and is theorized to reflect neural modifications associated with human psychostimulant addiction. While the mesolimbic dopaminergic pathway is known to play a role, the neurochemical mechanisms underlying behavioral sensitization remain incompletely understood. In this study, we conducted the first metabolomics analysis to globally characterize neurochemical differences associated with behavioral sensitization. Methamphetamine (MA)-induced sensitization measures were generated by statistically modeling longitudinal activity data for eight inbred strains of mice. Subsequent to behavioral testing, nontargeted liquid and gas chromatography-mass spectrometry profiling was performed on 48 brain samples, yielding 301 metabolite levels per sample after quality control. Association testing between metabolite levels and three primary dimensions of behavioral sensitization (total distance, stereotypy and margin time) showed four robust, significant associations at a stringent metabolome-wide significance threshold (false discovery rate, FDR biomarkers, and developing more comprehensive neurochemical models, of psychostimulant sensitization. © 2013 John Wiley & Sons Ltd and International Behavioural and Neural Genetics Society.

  8. Linking Essential Tremor to the Cerebellum: Neurochemical Evidence.

    Science.gov (United States)

    Marin-Lahoz, Juan; Gironell, Alexandre

    2016-06-01

    The pathophysiology and the exact anatomy of essential tremor (ET) is not well known. One of the pillars that support the cerebellum as the main anatomical locus in ET is neurochemistry. This review examines the link between neurochemical abnormalities found in ET and cerebellum. The review is based on published data about neurochemical abnormalities described in ET both in human and in animal studies. We try to link those findings with cerebellum. γ-aminobutyric acid (GABA) is the main neurotransmitter involved in the pathophysiology of ET. There are several studies about GABA that clearly points to a main role of the cerebellum. There are few data about other neurochemical abnormalities in ET. These include studies with noradrenaline, glutamate, adenosine, proteins, and T-type calcium channels. One single study reveals high levels of noradrenaline in the cerebellar cortex. Another study about serotonin neurotransmitter results negative for cerebellum involvement. Finally, studies on T-type calcium channels yield positive results linking the rhythmicity of ET and cerebellum. Neurochemistry supports the cerebellum as the main anatomical locus in ET. The main neurotransmitter involved is GABA, and the GABA hypothesis remains the most robust pathophysiological theory of ET to date. However, this hypothesis does not rule out other mechanisms and may be seen as the main scaffold to support findings in other systems. We clearly need to perform more studies about neurochemistry in ET to better understand the relations among the diverse systems implied in ET. This is mandatory to develop more effective pharmacological therapies.

  9. Benzodiazepine withdrawal: behavioural pharmacology and neurochemical changes.

    Science.gov (United States)

    File, S E; Andrews, N

    1993-01-01

    This paper describes pharmacological treatments that can reverse the anxiogenic response detected in animal tests when rats are withdrawn from chronic treatment with diazepam. Concurrent treatment with the calcium channel antagonist verapamil prevented this withdrawal response and the benzodiazepine-receptor antagonist flumazenil reversed the anxiogenic response and restored the system to a drug-naive state. Other treatments that reversed the anxiogenic response were the GABAB agonist baclofen, the 5-HT1A receptor agonist buspirone, and the 5-HT3 receptor antagonist (R,S)-zacopride (GABA = gamma-aminobutyric acid; 5-HT = 5-hydroxytryptamine). Both the enantiomers of zacopride contributed to this reversal. These behavioural reversals are interpreted in the light of biochemical studies showing increased 45Ca2+ flux and [3H]5-HT release from the hippocampus, during benzodiazepine withdrawal (Fig. 1).

  10. Neurobiology of addiction: insight from neurochemical imaging.

    Science.gov (United States)

    Urban, Nina B L; Martinez, Diana

    2012-06-01

    Neuroimaging studies have been crucial in understanding changes in the various neurotransmitter systems implicated in addiction in the living human brain. Predominantly reduced striatal dopamine transmission appears to play an important role in psychostimulant, alcohol and heroin addiction, while addiction to cannabis may be mediated primarily by the endocannabinoid system. However, the study of other neurotransmitter systems likely involved in addiction, for example glutamate, has been limited by the number and quality of available radiotracers, and data on changes in these systems in the most common addictions are emerging only now. Further studies are needed to understand fully how the interplay of various neurotransmitter systems contributes to addiction and to ultimately help to develop more effective treatment approaches.

  11. Expert recommendation: contributions to clinical practice of the new prodrug lisdexamfetamine dimesylate (LDX) in the treatment of attention deficit hyperactivity disorder (ADHD).

    Science.gov (United States)

    Alda, José A; Soutullo, César; Ramos-Quiroga, Josep A; Quintero, Javier; Hervás, Amaia; Hernández-Otero, Isabel; Sans-Fitó, Anna; Cardo-Jalón, Esther Cardo-Jalón; Fernández-Jaén, Alberto; Fernández-Pérez, Maximino; Hidalgo-Vicario, M Inés; Eddy-Ives, Lefa S; Sánchez, Javier

    2014-12-01

    Attention deficit hyperactivity disorder (ADHD) is one of the most common neurobiological disorders in childhood, and is characterized by inappropriate levels of inattention, hyperactivity and/or impulsiveness, with an estimated prevalence of 5.29%. ADHD can have a negative impact upon all areas of the life of the patient. The main clinical guides accept multimodal treatment, involving both pharmacological and psychological measures, as the best management approach in ADHD (psychoeducational, behavioural and academic). Lisdexamfetamine dimesylate (LDX) is a new drug for the treatment of ADHD. A multidiscipline expert document has been developed, compiling the scientific evidence referred to this new molecule. The study also addresses the existing shortcomings in current drug therapy for ADHD and the contributions of LDX to routine clinical practice, in an attempt to help and guide physicians in the use of this new treatment. This document is endorsed by the ADHD and Psychoeducational Development task Group of the Spanish Society of Primary Care Pediatrics (Grupo de TDAH y Desarrollo Psicoeducativo de la Asociación Española de Pediatría de Atención Primaria, AEPap), the Spanish Society of Pediatric Neurology (Sociedad Española de Neurología Pediátrica, SENEP) and the Spanish Society of Out-hospital Pediatrics and Primary Care (Sociedad Española de Pediatría Extrahospitalaria y Atención Primaria, SEPEAP).

  12. Youth Appraisals of Inter-parental Conflict and Genetic and Environmental Contributions to Attention-Deficit Hyperactivity Disorder: Examination of G×E Effects in a Twin Sample

    Science.gov (United States)

    Klump, Kelly L.; Burt, S. Alexandra

    2012-01-01

    Identification of gene × environment interactions (GxE) for attention-deficit hyperactivity disorder (ADHD) is a crucial component to understanding the mechanisms underpinning the disorder, as prior work indicates large genetic influences and numerous environmental risk factors. Building on prior research, children's appraisals of self-blame were examined as a psychosocial moderator of latent etiological influences on ADHD via biometric twin models, which provide an omnibus test of GxE while managing the potential confound of gene-environment correlation. Participants were 246 twin pairs (total n=492) ages 6–16 years. ADHD behaviors were assessed via mother report on the Child Behavior Checklist. To assess level of self-blame, each twin completed the Children's Perception of Inter-parental Conflict scale. Two biometric GxE models were fit to the data. The first model revealed a significant decrease in genetic effects and a significant increase in unique environmental influences on ADHD with increasing levels of self-blame. These results generally persisted even after controlling for confounding effects due to gene-environment correlation in the second model. Results suggest that appraisals of self-blame in relation to inter-parental conflict may act as a key moderator of etiological contributions to ADHD. PMID:22006350

  13. Metabolomics reveals distinct neurochemical profiles associated with stress resilience

    Directory of Open Access Journals (Sweden)

    Brooke N. Dulka

    2017-12-01

    Full Text Available Acute social defeat represents a naturalistic form of conditioned fear and is an excellent model in which to investigate the biological basis of stress resilience. While there is growing interest in identifying biomarkers of stress resilience, until recently, it has not been feasible to associate levels of large numbers of neurochemicals and metabolites to stress-related phenotypes. The objective of the present study was to use an untargeted metabolomics approach to identify known and unknown neurochemicals in select brain regions that distinguish susceptible and resistant individuals in two rodent models of acute social defeat. In the first experiment, male mice were first phenotyped as resistant or susceptible. Then, mice were subjected to acute social defeat, and tissues were immediately collected from the ventromedial prefrontal cortex (vmPFC, basolateral/central amygdala (BLA/CeA, nucleus accumbens (NAc, and dorsal hippocampus (dHPC. Ultra-high performance liquid chromatography coupled with high resolution mass spectrometry (UPLC-HRMS was used for the detection of water-soluble neurochemicals. In the second experiment, male Syrian hamsters were paired in daily agonistic encounters for 2 weeks, during which they formed stable dominant-subordinate relationships. Then, 24 h after the last dominance encounter, animals were exposed to acute social defeat stress. Immediately after social defeat, tissue was collected from the vmPFC, BLA/CeA, NAc, and dHPC for analysis using UPLC-HRMS. Although no single biomarker characterized stress-related phenotypes in both species, commonalities were found. For instance, in both model systems, animals resistant to social defeat stress also show increased concentration of molecules to protect against oxidative stress in the NAc and vmPFC. Additionally, in both mice and hamsters, unidentified spectral features were preliminarily annotated as potential targets for future experiments. Overall, these findings

  14. 'Whose atlas I use, his song I sing?' - The impact of anatomical atlases on fiber tract contributions to cognitive deficits after stroke.

    Science.gov (United States)

    de Haan, Bianca; Karnath, Hans-Otto

    2017-12-01

    Nowadays, different anatomical atlases exist for the anatomical interpretation of the results from neuroimaging and lesion analysis studies that investigate the contribution of white matter fiber tract integrity to cognitive (dys)function. A major problem with the use of different atlases in different studies, however, is that the anatomical interpretation of neuroimaging and lesion analysis results might vary as a function of the atlas used. This issue might be particularly prominent in studies that investigate the contribution of white matter fiber tract integrity to cognitive (dys)function. We used a single large-sample dataset of right brain damaged stroke patients with and without cognitive deficit (here: spatial neglect) to systematically compare the influence of three different, widely-used white matter fiber tract atlases (1 histology-based atlas and 2 DTI tractography-based atlases) on conclusions concerning the involvement of white matter fiber tracts in the pathogenesis of cognitive dysfunction. We both calculated the overlap between the statistical lesion analysis results and each long association fiber tract (topological analyses) and performed logistic regressions on the extent of fiber tract damage in each individual for each long association white matter fiber tract (hodological analyses). For the topological analyses, our results suggest that studies that use tractography-based atlases are more likely to conclude that white matter integrity is critical for a cognitive (dys)function than studies that use a histology-based atlas. The DTI tractography-based atlases classified approximately 10 times as many voxels of the statistical map as being located in a long association white matter fiber tract than the histology-based atlas. For hodological analyses on the other hand, we observed that the conclusions concerning the overall importance of long association fiber tract integrity to cognitive function do not necessarily depend on the white matter

  15. Changes in neurochemicals within the ventrolateral medullary respiratory column in awake goats after carotid body denervation

    Science.gov (United States)

    Miller, Justin Robert; Neumueller, Suzanne; Muere, Clarissa; Olesiak, Samantha; Pan, Lawrence; Hodges, Matthew R.

    2013-01-01

    A current and major unanswered question is why the highly sensitive central CO2/H+ chemoreceptors do not prevent hypoventilation-induced hypercapnia following carotid body denervation (CBD). Because perturbations involving the carotid bodies affect central neuromodulator and/or neurotransmitter levels within the respiratory network, we tested the hypothesis that after CBD there is an increase in inhibitory and/or a decrease in excitatory neurochemicals within the ventrolateral medullary column (VMC) in awake goats. Microtubules for chronic use were implanted bilaterally in the VMC within or near the pre-Bötzinger Complex (preBötC) through which mock cerebrospinal fluid (mCSF) was dialyzed. Effluent mCSF was collected and analyzed for neurochemical content. The goats hypoventilated (peak +22.3 ± 3.4 mmHg PaCO2) and exhibited a reduced CO2 chemoreflex (nadir, 34.8 ± 7.4% of control ΔV̇E/ΔPaCO2) after CBD with significant but limited recovery over 30 days post-CBD. After CBD, GABA and glycine were above pre-CBD levels (266 ± 29% and 189 ± 25% of pre-CBD; P 0.05) different from control after CBD. Analyses of brainstem tissues collected 30 days after CBD exhibited 1) a midline raphe-specific reduction (P < 0.05) in the percentage of tryptophan hydroxylase–expressing neurons, and 2) a reduction (P < 0.05) in serotonin transporter density in five medullary respiratory nuclei. We conclude that after CBD, an increase in inhibitory neurotransmitters and a decrease in excitatory neuromodulation within the VMC/preBötC likely contribute to the hypoventilation and attenuated ventilatory CO2 chemoreflex. PMID:23869058

  16. Faster Forgetting Contributes to Impaired Spatial Memory in the PDAPP Mouse: Deficit in Memory Retrieval Associated with Increased Sensitivity to Interference?

    Science.gov (United States)

    Daumas, Stephanie; Sandin, Johan; Chen, Karen S.; Kobayashi, Dione; Tulloch, Jane; Martin, Stephen J.; Games, Dora; Morris, Richard G. M.

    2008-01-01

    Two experiments were conducted to investigate the possibility of faster forgetting by PDAPP mice (a well-established model of Alzheimer's disease as reported by Games and colleagues in an earlier paper). Experiment 1, using mice aged 13-16 mo, confirmed the presence of a deficit in a spatial reference memory task in the water maze by hemizygous…

  17. Youth Appraisals of Inter-Parental Conflict and Genetic and Environmental Contributions to Attention-Deficit Hyperactivity Disorder: Examination of GxE Effects in a Twin Sample

    Science.gov (United States)

    Nikolas, Molly; Klump, Kelly L.; Burt, S. Alexandra

    2012-01-01

    Identification of gene x environment interactions (GxE) for attention-deficit hyperactivity disorder (ADHD) is a crucial component to understanding the mechanisms underpinning the disorder, as prior work indicates large genetic influences and numerous environmental risk factors. Building on prior research, children's appraisals of self-blame were…

  18. Relative contribution of attention-deficit hyperactivity disorder, obsessive-compulsive disorder, and tic severity to social and behavioral problems in tic disorders

    NARCIS (Netherlands)

    Hoekstra, PJ; Steenhuis, MP; Troost, PW; Korf, J; Kallenberg, CGM; Minderaa, RB

    The aim of this study was to investigate social and behavioral problems related to attention-deficit hyperactivity disorder (ADHD), obsessions and compulsions, and tic severity in children with a tic disorder. Parents of 58 children with a tic disorder with and without different forms of ADHD

  19. Using position emission tomography to investigate hormone-mediated neurochemical changes across the female lifespan: implications for depression.

    Science.gov (United States)

    Zsido, Rachel G; Villringer, Arno; Sacher, Julia

    2017-12-01

    Ovarian hormones, particularly oestrogen and progesterone, undergo major fluctuations across the female lifespan. These hormone transition periods, such as the transition from pregnancy to postpartum, as well as the transition into menopause (perimenopause), are also known to be times of elevated susceptibility to depression. This study reviews how these transition periods likely influence neurochemical changes in the brain that result in disease vulnerability. While there are known associations between oestrogen/progesterone and different monoaminergic systems, the interactions and their potential implications for mood disorders are relatively unknown. Positron Emission Tomography (PET) allows for the in-vivo quantification of such neurochemical changes, and, thus, can provide valuable insight into how both subtle and dramatic shifts in hormones contribute to the elevated rates of depression during pre-menstrual, post-partum, and perimenopausal periods in a woman's life. As one better understands how to address the challenges of PET studies involving highly vulnerable populations, such as women who have recently given birth, one will gain the insight necessary to design and individualize treatment and therapy. Understanding the precise time-line in younger women when dramatic fluctuations in the hormonal milieu may contribute to brain changes may present a powerful opportunity to intervene before a vulnerable state develops into a diseased state in later life.

  20. Clozapine protection against gestational cocaine-induced neurochemical abnormalities.

    Science.gov (United States)

    Yablonsky-Alter, Elena; Gashi, Eleonora; Lidsky, Theodore I; Wang, Hoau-Yan; Banerjee, Shailesh P

    2005-01-01

    Clozapine was found to be effective in attenuating cocaine-induced neurochemical effects. We investigate whether clozapine influences in utero cocaine exposure-induced changes in striatal dopamine levels and cortical N-methyl-D-aspartate (NMDA) receptor density in mouse and rat brains. Pregnant mice or rats were injected with cocaine (5 or 10 mg/kg intraperitoneally) or saline every 24 h throughout gestation and continued for 6 weeks following the delivery. Striatal dopamine levels measured by high-pressure liquid chromatography were found to decrease 24 to 33% in gestational cocaine exposed between the ages of 3 to 15 days, but not in 42-day-old pups. The cortical NMDA receptor densities assessed either in the presence of 100 microM glutamate or 30 microM glycine were significantly increased in 15-day-old gestational cocaine-exposed rats. Simultaneous daily administration of 3 mg/kg clozapine with 5 mg/kg cocaine to pregnant mice protected against the decrease in striatal dopamine levels or an increase in the concentration of NMDA receptor measured in the presence of 100 microM glutamate in 15-day-old pups. Clozapine did not affect striatal dopamine levels by itself or when coadministered with cocaine in 42-day-old pups. The results show gestational cocaine may induce neurochemical abnormalities in brain exhibited as an increased glutamate NMDA receptor density together with a decreased striatal dopamine level. These effects of gestational cocaine exposure may be prevented by simultaneous administration of clozapine. Thus clozapine, which is a partial agonist at the NMDA receptor, may be of value in protecting against gestational cocaine-induced adverse effects in the brain.

  1. Water Deficit Enhances C Export to the Roots in Arabidopsis thaliana Plants with Contribution of Sucrose Transporters in Both Shoot and Roots1[OPEN

    Science.gov (United States)

    Durand, Mickaël; Porcheron, Benoît; Maurousset, Laurence; Lemoine, Rémi; Pourtau, Nathalie

    2016-01-01

    Root high plasticity is an adaptation to its changing environment. Water deficit impairs growth, leading to sugar accumulation in leaves, part of which could be available to roots via sucrose (Suc) phloem transport. Phloem loading is widely described in Arabidopsis (Arabidopsis thaliana), while unloading in roots is less understood. To gain information on leaf-to-root transport, a soil-based culture system was developed to monitor root system architecture in two dimensions. Under water deficit (50% of soil water-holding capacity), total root length was strongly reduced but the depth of root foraging and the shape of the root system were less affected, likely to improve water uptake. 14CO2 pulse-chase experiments confirmed that water deficit enhanced carbon (C) export to the roots, as suggested by the increased root-to-shoot ratio. The transcript levels of AtSWEET11 (for sugar will eventually be exported transporter), AtSWEET12, and AtSUC2 (for Suc carrier) genes, all three involved in Suc phloem loading, were significantly up-regulated in leaves of water deficit plants, in accordance with the increase in C export from the leaves to the roots. Interestingly, the transcript levels of AtSUC2 and AtSWEET11 to AtSWEET15 were also significantly higher in stressed roots, underlying the importance of Suc apoplastic unloading in Arabidopsis roots and a putative role for these Suc transporters in Suc unloading. These data demonstrate that, during water deficit, plants respond to growth limitation by allocating relatively more C to the roots to maintain an efficient root system and that a subset of Suc transporters is potentially involved in the flux of C to and in the roots. PMID:26802041

  2. Water Deficit Enhances C Export to the Roots in Arabidopsis thaliana Plants with Contribution of Sucrose Transporters in Both Shoot and Roots.

    Science.gov (United States)

    Durand, Mickaël; Porcheron, Benoît; Hennion, Nils; Maurousset, Laurence; Lemoine, Rémi; Pourtau, Nathalie

    2016-03-01

    Root high plasticity is an adaptation to its changing environment. Water deficit impairs growth, leading to sugar accumulation in leaves, part of which could be available to roots via sucrose (Suc) phloem transport. Phloem loading is widely described in Arabidopsis (Arabidopsis thaliana), while unloading in roots is less understood. To gain information on leaf-to-root transport, a soil-based culture system was developed to monitor root system architecture in two dimensions. Under water deficit (50% of soil water-holding capacity), total root length was strongly reduced but the depth of root foraging and the shape of the root system were less affected, likely to improve water uptake. (14)CO2 pulse-chase experiments confirmed that water deficit enhanced carbon (C) export to the roots, as suggested by the increased root-to-shoot ratio. The transcript levels of AtSWEET11 (for sugar will eventually be exported transporter), AtSWEET12, and AtSUC2 (for Suc carrier) genes, all three involved in Suc phloem loading, were significantly up-regulated in leaves of water deficit plants, in accordance with the increase in C export from the leaves to the roots. Interestingly, the transcript levels of AtSUC2 and AtSWEET11 to AtSWEET15 were also significantly higher in stressed roots, underlying the importance of Suc apoplastic unloading in Arabidopsis roots and a putative role for these Suc transporters in Suc unloading. These data demonstrate that, during water deficit, plants respond to growth limitation by allocating relatively more C to the roots to maintain an efficient root system and that a subset of Suc transporters is potentially involved in the flux of C to and in the roots. © 2016 American Society of Plant Biologists. All Rights Reserved.

  3. [Correlation of neurochemical metabolism with memory function in young adult patients with first-episode depression studied with proton magnetic resonance spectroscopy].

    Science.gov (United States)

    Liu, Weibo; Yu, Hualiang; Jiang, Biao; Zheng, Leilei; Yu, Shaohua; Pan, Bing; Yu, Risheng

    2013-07-01

    To investigate the correlation of neurochemical metabolism in hippocampus with memory function in young adult patients with first-episode depression. Twenty patients with first-episode depression (patient group) and fifteen health subjects (control group) were enrolled in the study. The neurochemical metabolism, including the levels of N-acetylaspartate (NAA), Choline (Cho), Creatine (Cr), Myoinositol (mI) were measured by proton magnetic resonance spectroscope (1H-MRS) in bilateral hippocampus. Wechsler Memory Scale (WMS) were used to examine the memory function in both groups. The memory quotient (89.15 ±6.62) of patient group was significantly lower than that of controls (P memory,short-term memory and immediate memory in patients were also lower than those of controls (Pmemory deficit and abnormal metabolism function of neuron cell in hippocampus coexist in young adult patients with first-episode depression, and the lower NAA/Cr and higher mI/Cr ratio in the left hippocampus may result in the memory deficit.

  4. Nitric oxide synthase and arginase expression changes in the rat perirhinal and entorhinal cortices following unilateral vestibular damage: a link to deficits in object recognition?

    Science.gov (United States)

    Liu, Ping; Gliddon, Catherine M; Lindsay, Libby; Darlington, Cynthia L; Smith, Paul F

    2004-01-01

    Previous studies have shown that peripheral vestibular damage causes long-term neurochemical changes in the hippocampus which may be related to spatial memory deficits. Since recent studies have also demonstrated deficits in non-spatial object recognition memory following vestibular lesions, the aim of the present study was to extend these investigations into the perirhinal cortex (PRC), which is known to be important for object recognition, and the related entorhinal cortex (EC). We examined the effects of unilateral vestibular deafferentation (UVD) on the expression of four enzymes associated with neuronal plasticity, neuronal nitric oxide synthase (nNOS), endothelial nitric oxide synthase (eNOS), arginase I and arginase II (AI and II), in the rat EC and PRC using Western blotting. Tissue was collected at 10 hs, 50 hs and 2 weeks post-UVD. In the EC and PRC, nNOS protein expression decreased on the contralateral side at 2 weeks post-UVD but not before. At the same time, eNOS protein expression increased in both regions on the contralateral side. In the EC, AII protein expression increased on the ipsilateral side at 2 weeks post-UVD. In the PRC, AI increased and decreased on the contralateral and ipsilateral sides (respectively) at 2 weeks post-UVD. AII showed a bilateral increase in the PRC at 2 weeks post-UVD. These results demonstrate changes in NOS and arginase protein expression in the PRC and EC following UVD, which are unlikely to be due to the initial severity of the vestibular syndrome because they develop well after vestibular compensation has taken place. Neurochemical changes in these regions of the medial temporal lobe may be implicated in the development of object recognition deficits that contribute to cognitive dysfunction following peripheral vestibular damage.

  5. Neurochemical phenotype of cytoglobin‑expressing neurons in the rat hippocampus

    DEFF Research Database (Denmark)

    Hundahl, Christian Ansgar; Fahrenkrug, Jan; Hannibal, Jens

    2014-01-01

    of Cygb neurons remain uncharacterized by the neurochemical content. The aim of the present study was to provide an additional and more detailed neurochemical phenotype of Cygb-expressing neurons in the rat hippocampus. The rat hippocampus was chosen due to the abundance of Cygb, as well as this limbic...... of Cygb neurons co-expressing nNOS. Furthermore, it was shown that the majority of neurons expressing somastostatin and vasoactive intestinal peptide also co-express Cygb and nNOS. Detailed information regarding the neurochemical phenotype of Cygb neurons in the hippocampus can be a valuable tool...

  6. The contribution of discrete-trial naming and visual recognition to rapid automatized naming deficits of dyslexic children with and without a history of language delay

    Directory of Open Access Journals (Sweden)

    Filippo eGasperini

    2014-09-01

    Full Text Available Children with Developmental Dyslexia (DD are impaired in Rapid Automatized Naming (RAN tasks, where subjects are asked to name arrays of high frequency items as quickly as possible. However the reasons why RAN speed discriminates DD from typical readers are not yet fully understood. Our study was aimed to identify some of the cognitive mechanisms underlying RAN-reading relationship by comparing one group of 32 children with DD with an age-matched control group of typical readers on a naming and a visual recognition task both using a discrete-trial methodology , in addition to a serial RAN task, all using the same stimuli (digits and colors. Results showed a significant slowness of DD children in both serial and discrete-trial naming tasks regardless of type of stimulus, but no difference between the two groups on the discrete-trial recognition task. Significant differences between DD and control participants in the RAN task disappeared when performance in the discrete-trial naming task was partialled out by covariance analysis for colors, but not for digits. The same pattern held in a subgroup of DD subjects with a history of early language delay (LD. By contrast, in a subsample of DD children without LD the RAN deficit was specific for digits and disappeared after slowness in discrete-trial naming was partialled out. Slowness in discrete-trial naming was more evident for LD than for noLD DD children. Overall, our results confirm previous evidence indicating a name-retrieval deficit as a cognitive impairment underlying RAN slowness in DD children. This deficit seems to be more marked in DD children with previous LD. Moreover, additional cognitive deficits specifically associated with serial RAN tasks have to be taken into account when explaining deficient RAN speed of these latter children. We suggest that partially different cognitive dysfunctions underpin superficially similar RAN impairments in different subgroups of DD subjects.

  7. Differential contribution of APP metabolites to early cognitive deficits in a TgCRND8 mouse model of Alzheimer’s disease

    Science.gov (United States)

    Hamm, Valentine; Héraud, Céline; Bott, Jean-Bastien; Herbeaux, Karine; Strittmatter, Carole; Mathis, Chantal; Goutagny, Romain

    2017-01-01

    Alzheimer’s disease (AD) is a neurodegenerative pathology commonly characterized by a progressive and irreversible deterioration of cognitive functions, especially memory. Although the etiology of AD remains unknown, a consensus has emerged on the amyloid hypothesis, which posits that increased production of soluble amyloid β (Aβ) peptide induces neuronal network dysfunctions and cognitive deficits. However, the relative failures of Aβ-centric therapeutics suggest that the amyloid hypothesis is incomplete and/or that the treatments were given too late in the course of AD, when neuronal damages were already too extensive. Hence, it is striking to see that very few studies have extensively characterized, from anatomy to behavior, the alterations associated with pre-amyloid stages in mouse models of AD amyloid pathology. To fulfill this gap, we examined memory capacities as well as hippocampal network anatomy and dynamics in young adult pre-plaque TgCRND8 mice when hippocampal Aβ levels are still low. We showed that TgCRND8 mice present alterations in hippocampal inhibitory networks and γ oscillations at this stage. Further, these mice exhibited deficits only in a subset of hippocampal-dependent memory tasks, which are all affected at later stages. Last, using a pharmacological approach, we showed that some of these early memory deficits were Aβ-independent. Our results could partly explain the limited efficacy of Aβ-directed treatments and favor multitherapy approaches for early symptomatic treatment for AD. PMID:28275722

  8. Behavioral and Neurochemical Studies in Stressed and Unstressed Rats Fed on Protein, Carbohydrate and Fat Rich Diet

    Directory of Open Access Journals (Sweden)

    Samia Moin§, Saida Haider*, Saima Khaliq1, Saiqa Tabassum and Darakhshan J. Haleem

    2012-05-01

    Full Text Available Stress produces behavioral and neurochemical deficits. To study the relationship between adaptation to stress and macronutrient intake, the present study was designed to monitor the effects of different diets on feed intake, growth rate and serotonin (5-Hydroxytryptamine, 5-HT metabolism following exposure to restraint stress in rats. Rats were divided into four groups (n=12 as control, sugar, protein and fat rich diet fed rats. After 5 weeks of treatment animals of each group were divided into unrestrained and restrained animals (n=6. Rats of restrained group were given immobilization stress for 2 hours/day for 5 days. Food intake and growth rates of unrestrained and restrained rats were monitored daily. Rats were decapitated on 6th day to collect brain samples for neurochemical estimation. Results show that sugar diet fed rats produced adaptation to stress early as compared to normal diet fed rats. Food intake and growth rates of unrestrained and restrained rats were comparable on 3rd day in sugar diet fed rats and on 4th day in normal diet fed rats. Stress decreased food intake and growth rates of protein and fat treated rats. Repeated stress did not alter brain 5-HT and 5-HIAA levels of normal diet fed rats and sugar diet fed rats. Protein diet fed restrained rats showed elevated brain 5-HT levels. Fat diet fed restrained rats significantly decreased brain TRP and 5-HIAA levels. Finding suggested that carbohydrate diet might protect against stressful conditions. Study also showed that nutritional status could alter different behaviors in response to a stressful environment.

  9. NMR-Based Metabolic Profiling Reveals Neurochemical Alterations in the Brain of Rats Treated with Sorafenib.

    Science.gov (United States)

    Du, Changman; Shao, Xue; Zhu, Ruiming; Li, Yan; Zhao, Qian; Fu, Dengqi; Gu, Hui; Kong, Jueying; Luo, Li; Long, Hailei; Deng, Pengchi; Wang, Huijuan; Hu, Chunyan; Zhao, Yinglan; Cen, Xiaobo

    2015-11-01

    Sorafenib, an active multi-kinase inhibitor, has been widely used as a chemotherapy drug to treat advanced clear-cell renal cell carcinoma patients. In spite of the relative safety, sorafenib has been shown to exert a negative impact on cognitive functioning in cancer patients, specifically on learning and memory; however, the underlying mechanism remains unclear. In this study, an NMR-based metabolomics approach was applied to investigate the neurochemical effects of sorafenib in rats. Male rats were once daily administrated with 120 mg/kg sorafenib by gavage for 3, 7, and 28 days, respectively. NMR-based metabolomics coupled with histopathology examinations for hippocampus, prefrontal cortex (PFC), and striatum were performed. The (1)H NMR spectra data were analyzed by using multivariate pattern recognition techniques to show the time-dependent biochemical variations induced by sorafenib. Excellent separation was obtained and distinguishing metabolites were observed between sorafenib-treated and control rats. A total of 36 differential metabolites in hippocampus of rats treated with sorafenib were identified, some of which were significantly changed. Furthermore, these modified metabolites mainly reflected the disturbances in neurotransmitters, energy metabolism, membrane, and amino acids. However, only a few metabolites in PFC and striatum were altered by sorafenib. Additionally, no apparent histological changes in these three brain regions were observed in sorafenib-treated rats. Together, our findings demonstrate the disturbed metabonomics pathways, especially, in hippocampus, which may underlie the sorafenib-induced cognitive deficits in patients. This work also shows the advantage of NMR-based metabolomics over traditional approach on the study of biochemical effects of drugs.

  10. Neuroendocrine and neurochemical impact of aggressive social interactions in submissive and dominant mice: implications for stress-related disorders.

    Science.gov (United States)

    Audet, Marie-Claude; Anisman, Hymie

    2010-04-01

    Social conflicts may engender stress-related behavioural and physiological disturbances in the victims of aggression. In addition, stress-like neurochemical changes and ensuing depressive and anxiety symptoms might also be evident in the perpetrators of aggressive acts. The present investigation assessed basal levels of circulating corticosterone and of brain serotonin (5-HT) and norepinephrine (NE) in pre-identified submissive and dominant mice. In addition, brain neurochemical changes were determined following a single or three 15-min aggressive episodes both in submissive mice and in those that dominated the aggressive interplay. Three minutes after single and repeated confrontations, plasma corticosterone levels and 5-HT utilization within the prefrontal cortex (PFC) and hippocampus were increased to a comparable extent in submissive and dominant animals. Interestingly, however, NE utilization within the PFC and hippocampus was augmented to a greater level in submissive mice. These results suggest that 5-HT neuronal functioning was generally responsive to aggressive events, irrespective of social rank, whereas NE neuronal activity within the PFC and hippocampus was more sensitive to the submissive/dominance attributes of the social situation. It is possible that NE and 5-HT variations associated with an aggressive experience contribute to depressive- and anxiety-like manifestations typically observed after such psychosocial stressors, particularly in submissive mice. However, given that 5-HT changes occur irrespective of social rank, these data suggest that a toll is taken on both submissive and dominant mice, leaving them vulnerable to stress-related pathology.

  11. Comparison of Different Matrices as Potential Quality Control Samples for Neurochemical Dementia Diagnostics

    NARCIS (Netherlands)

    Lelental, N.; Brandner, S.; Kofanova, O.; Blennow, K.; Zetterberg, H.; Andreasson, U.; Engelborghs, S.; Mroczko, B.; Gabryelewicz, T.; Teunissen, C.; Mollenhauer, B.; Parnetti, L.; Chiasserini, D.; Molinuevo, J.L.; Perret-Liaudet, A.; Verbeek, M.M.; Andreasen, N.; Brosseron, F.; Bahl, J.M.; Herukka, S.K.; Hausner, L.; Frolich, L.; Labonte, A.; Poirier, J.; Miller, A.M.; Zilka, N.; Kovacech, B.; Urbani, A.; Suardi, S.; Oliveira, C. de; Baldeiras, I.; Dubois, B.; Rot, U.; Lehmann, S.; Skinningsrud, A.; Betsou, F.; Wiltfang, J.; Gkatzima, O.; Winblad, B.; Buchfelder, M.; Kornhuber, J.; Lewczuk, P.

    2016-01-01

    BACKGROUND: Assay-vendor independent quality control (QC) samples for neurochemical dementia diagnostics (NDD) biomarkers are so far commercially unavailable. This requires that NDD laboratories prepare their own QC samples, for example by pooling leftover cerebrospinal fluid (CSF) samples.

  12. Comparison of Different Matrices as Potential Quality Control Samples for Neurochemical Dementia Diagnostics

    NARCIS (Netherlands)

    Lelental, Natalia; Brandner, Sebastian; Kofanova, Olga; Blennow, Kaj; Zetterberg, Henrik; Andreasson, Ulf; Engelborghs, Sebastiaan; Mroczko, Barbara; Gabryelewicz, Tomasz; Teunissen, Charlotte; Mollenhauer, Brit; Parnetti, Lucilla; Chiasserini, Davide; Molinuevo, Jose Luis; Perret-Liaudet, Armand; Verbeek, Marcel M.; Andreasen, Niels; Brosseron, Frederic; Bahl, Justyna M. C.; Herukka, Sanna-Kaisa; Hausner, Lucrezia; Froelich, Lutz; Labonte, Anne; Poirier, Judes; Miller, Anne-Marie; Zilka, Norbert; Kovacech, Branislav; Urbani, Andrea; Suardi, Silvia; Oliveira, Catarina; Baldeiras, Ines; Dubois, Bruno; Rot, Uros; Lehmann, Sylvain; Skinningsrud, Anders; Betsou, Fay; Wiltfang, Jens; Gkatzima, Olymbia; Winblad, Bengt; Buchfelder, Michael; Kornhuber, Johannes; Lewczuk, Piotr

    2016-01-01

    Background: Assay-vendor independent quality control (QC) samples for neurochemical dementia diagnostics (NDD) biomarkers are so far commercially unavailable. This requires that NDD laboratories prepare their own QC samples, for example by pooling leftover cerebrospinal fluid (CSF) samples.

  13. Neurochemical Effects of Chronic Administration of Calcitriol in Rats

    Directory of Open Access Journals (Sweden)

    Pei Jiang

    2014-12-01

    Full Text Available Despite accumulating data showing the various neurological actions of vitamin D (VD, its effects on brain neurochemistry are still far from fully understood. To further investigate the neurochemical influence of VD, we assessed neurotransmitter systems in the brain of rats following 6-week calcitriol (1,25-dihydroxyvitamin D administration (50 ng/kg/day or 100 ng/kg/day. Both the two doses of calcitriol enhanced VDR protein level without affecting serum calcium and phosphate status. Rats treated with calcitriol, especially with the higher dose, exhibited elevated γ-aminobutyric acid (GABA status. Correspondingly, the mRNA expression of glutamate decarboxylase (GAD 67 was increased. 100 ng/kg of calcitriol administration also increased glutamate and glutamine levels in the prefrontal cortex, but did not alter glutamine synthetase (GS expression. Additionally, calcitriol treatment promoted tyrosine hydroxylase (TH and tryptophan hydroxylase 2 (TPH2 expression without changing dopamine and serotonin status. However, the concentrations of the metabolites of dopamine and serotonin were increased and the drug use also resulted in a significant rise of monoamine oxidase A (MAOA expression, which might be responsible to maintain the homeostasis of dopaminergic and serotonergic neurotransmission. Collectively, the present study firstly showed the effects of calcitriol in the major neurotransmitter systems, providing new evidence for the role of VD in brain function.

  14. A neurochemical approach to valuation sensitivity over gains and losses.

    Science.gov (United States)

    Zhong, Songfa; Israel, Salomon; Xue, Hong; Sham, Pak C; Ebstein, Richard P; Chew, Soo Hong

    2009-12-07

    Prospect theory proposes the hypothesis that people have diminishing sensitivity in valuing increases in the size of monetary outcomes, for both gains and losses. For decision-making under risk, this implies a tendency to be risk-tolerant over losses while being generally risk averse over gains. We offer a neurochemistry-based model of the diminishing valuation sensitivity hypothesis. Specifically, we propose that dopamine tone modulates the sensitivity towards valuation of gains while serotonin tone modulates the sensitivity towards valuation of losses. Consequently, higher dopamine tone would yield a more concave valuation function over gains while higher serotonin tone would yield a more convex valuation function over losses. Using a neurogenetics strategy to test our neurochemical model, we find that subjects with the 9-repeat allele of DAT1 (lower DA tone) are more risk-tolerant over gains than subjects with the 10-repeat allele, and that subjects with the 10-repeat allele of STin2 (higher 5HT tone) are more risk-tolerant over losses than subjects with the 12-repeat allele. Overall, our results support the implications of our model and provide the first neurogenetics evidence that risk attitudes are partially hard-wired in differentiating between gain- and loss-oriented risks.

  15. Neurochemical Alterations in Sudden Unexplained Perinatal Deaths—A Review

    Directory of Open Access Journals (Sweden)

    Nazeer Muhammad

    2018-01-01

    Full Text Available Sudden unexpected perinatal collapse is a major trauma for the parents of victims. Sudden infant death syndrome (SIDS is unexpected and mysterious death of an apparently healthy neonate from birth till 1 year of age without any known causes, even after thorough postmortem investigations. However, the incidence of sudden intrauterine unexplained death syndrome (SIUDS is seven times higher as compared with SIDS. This observation is approximated 40–80%. Stillbirth is defined as death of a fetus after 20th week of gestation or just before delivery at full term without a known reason. Pakistan has the highest burden of stillbirth in the world. This basis of SIDS, SIUDS, and stillbirths eludes specialists. The purpose of this study is to investigate factors behind failure in control of these unexplained deaths and how research may go ahead with improved prospects. Animal models and physiological data demonstrate that sleep, arousal, and cardiorespiratory malfunctioning are abnormal mechanisms in SIUDS risk factors or in newborn children who subsequently die from SIDS. This review focuses on insights in neuropathology and mechanisms of SIDS and SIUDS in terms of different receptors involved in this major perinatal demise. Several studies conducted in the past decade have confirmed neuropathological and neurochemical anomalies related to serotonin transporter, substance P, acetylcholine α7 nicotine receptors, etc., in sudden unexplained fetal and infant deaths. There is need to focus more on research in this area to unveil the major curtain to neuroprotection by underlying mechanisms leading to such deaths.

  16. Dyslipidemia links obesity to early cerebral neurochemical alterations.

    Science.gov (United States)

    Haley, Andreana P; Gonzales, Mitzi M; Tarumi, Takashi; Tanaka, Hirofumi

    2013-10-01

    To examine the role of hypertension, hyperglycemia, and dyslipidemia in potentially accounting for obesity-related brain vulnerability in the form of altered cerebral neurochemistry. Sixty-four adults, ages 40-60 years, underwent a health screen and proton magnetic resonance spectroscopy ((1) H MRS) of occipitoparietal gray matter to measure N-acetyl aspartate (NAA), choline (Cho), myo-inositol (mI), and glutamate (Glu) relative to creatine (Cr). The causal steps approach and nonparametric bootstrapping were utilized to assess if fasting glucose, mean arterial pressure or peripheral lipid/lipoprotein levels mediate the relationship between body mass index (BMI) and cerebral neurochemistry. Higher BMI was significantly related to higher mI/Cr, independent of age and sex. BMI was also significantly related to two of the proposed mediators, triglyceride, and HDL-cholesterol, which were also independently related to increased mI/Cr. Finally, the relationship between BMI and mI/Cr was significantly attenuated after inclusion of triglyceride and HDL-cholesterol into the model, one at a time, indicating statistical mediation. Higher triglyceride and lower HDL levels statistically account for the association between BMI and myo-inositol, pointing toward a potentially critical role for dyslipidemia in the development of cerebral neurochemical alterations in obesity. Copyright © 2013 The Obesity Society.

  17. Neurochemical background and approaches in the understanding of motion sickness

    Science.gov (United States)

    Kohl, R. L.

    1982-01-01

    The problems and nature of space motion sickness were defined. The neurochemical and neurophysiological bases of vestibular system function and of the expression of motion sickness wre reviewed. Emphasis was given to the elucidation of the neuropharmacological mechanisms underlying the effects of scopolamine and amphetamine on motion sickness. Characterization of the ascending reticular activating system and the limbic system provided clues to the etiology of the side effects of scopolamine. The interrelationship between central cholinergic pathways and the peripheral (autonomic) expression of motion sickness was described. A correlation between the stress of excessive motion and a variety of hormonal responses to that stress was also detailed. The cholinergic system is involved in the efferent modulation of the vestibular hair cells, as an afferent modulator of the vestibular nuclei, in the activation of cortical and limbic structures, in the expression of motion sickness symptoms and most likely underscores a number of the hormonal changes that occur in stressful motion environments. The role of lecithin in the regulation of the levels of neurotransmitters was characterized as a possible means by which cholinergic neurochemistry can be modulated.

  18. Social Stress and Psychosis Risk: Common Neurochemical Substrates?

    Science.gov (United States)

    Mizrahi, Romina

    2016-02-01

    Environmental risk factors have been implicated in the etiology of psychotic disorders, with growing evidence showing the adverse effects of migration, social marginalization, urbanicity, childhood trauma, social defeat, and other adverse experiences on mental health in vulnerable populations. Collectively, social stress may be one mechanism that could link these environmental risk factors. The exact mechanism(s) by which social stress can affect brain function, and in particular the molecular targets involved in psychosis (such as the dopaminergic (DA) system), is (are) not fully understood. In this review, we will discuss the interplay between social environmental risk factors and molecular changes in the human brain; in particular, we will highlight the impact of social stress on three specific neurochemical systems: DA, neuroinflammation/immune, and endocannabinoid (eCB) signaling. We have chosen the latter two molecular pathways based on emerging evidence linking schizophrenia to altered neuroinflammatory processes and cannabis use. We further identify key developmental periods in which social stress interacts with these pathways, suggesting window(s) of opportunities for novel interventions. Taken together, we suggest that they may have a key role in the pathogenesis and disease progression, possibly provide novel treatment options for schizophrenia, and perhaps even prevent it.

  19. Neurochemical consequence of steroid abuse: stanozolol-induced monoaminergic changes.

    Science.gov (United States)

    Tucci, Paolo; Morgese, Maria Grazia; Colaianna, Marilena; Zotti, Margherita; Schiavone, Stefania; Cuomo, Vincenzo; Trabace, Luigia

    2012-02-01

    An extensive literature has documented adverse effects on mental health in anabolic androgenic steroids (AAS) abusers. Depression seems a common adverse reaction in AAS abusers. Recently it has been reported that in a rat model of AAS abuse stanozolol induces behavioural and biochemical changes related to the pathophysiology of major depressive disorder. In the present study, we used the model of AAS abuse to examine possible changes in the monoaminergic system, a neurobiological substrate of depression, in different brain areas of stanozolol-treated animals. Wistar rats received repeated injections of stanozolol (5mg/kg, s.c.), or vehicle (propylene glycol, 1ml/kg) once daily for 4weeks. Twenty-four hours after last injection, changes of dopamine (DA) and relative metabolite levels, homovanilic acid (HVA) and 3,4-dihydroxy phenylacetic acid (DOPAC), serotonin (5-HT) and its metabolite levels, 5-hydroxy indolacetic acid (5-HIAA), and noradrenaline (NA) amount were investigated in prefrontal cortex (PFC), nucleus accumbens (NAC), striatum (STR) and hippocampus (HIPP). The analysis of data showed that after chronic stanozolol, DA levels were increased in the HIPP and decreased in the PFC. No significant changes were observed in the STR or in the NAC. 5-HT and 5-HIAA levels were decreased in all brain areas investigated after stanozolol exposure; however, the 5-HIAA/5-HT ratio was not altered. Taken together, our data indicate that chronic use of stanozolol significantly affects brain monoamines leading to neurochemical modifications possibly involved in depression and stress-related states. Copyright © 2011 Elsevier Inc. All rights reserved.

  20. Neurochemical organization of the nucleus paramedianus dorsalis in the human.

    Science.gov (United States)

    Baizer, Joan S; Baker, James F; Haas, Kristin; Lima, Raquel

    2007-10-24

    We have characterized the neurochemical organization of a small brainstem nucleus in the human brain, the nucleus paramedianus dorsalis (PMD). PMD is located adjacent and medial to the nucleus prepositus hypoglossi (PH) in the dorsal medulla and is distinguished by the pattern of immunoreactivity of cells and fibers to several markers including calcium-binding proteins, a synthetic enzyme for nitric oxide (neuronal nitric oxide synthase, nNOS) and a nonphosphorylated neurofilament protein (antibody SMI-32). In transverse sections, PMD is oval with its long axis aligned with the dorsal border of the brainstem. We identified PMD in eight human brainstems, but found some variability both in its cross-sectional area and in its A-P extent among cases. It includes calretinin immunoreactive large cells with oval or polygonal cell bodies. Cells in PMD are not immunoreactive for either calbindin or parvalbumin, but a few fibers immunoreactive to each protein are found within its central region. Cells in PMD are also immunoreactive to nNOS, and immunoreactivity to a neurofilament protein shows many labeled cells and fibers. No similar region is identified in atlases of the cat, mouse, rat or monkey brain, nor does immunoreactivity to any of the markers that delineate it in the human reveal a comparable region in those species. The territory that PMD occupies is included in PH in other species. Since anatomical and physiological data in animals suggest that PH may have multiple subregions, we suggest that the PMD in human may be a further differentiation of PH and may have functions related to the vestibular control of eye movements.

  1. Neurochemical Evidence of Potential Neurotoxicity After Prophylactic Cranial Irradiation

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    Kalm, Marie, E-mail: marie.kalm@neuro.gu.se [Department of Clinical Neuroscience and Rehabilitation, Insitute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg (Sweden); Abel, Edvard [Department of Oncology, Institute of Clinical Sciences, Sahlgrenska Academy at the University of Gothenburg, Gothenburg (Sweden); Wasling, Pontus [Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg (Sweden); Nyman, Jan [Department of Oncology, Institute of Clinical Sciences, Sahlgrenska Academy at the University of Gothenburg, Gothenburg (Sweden); Hietala, Max Albert [Department of Neurology, Karolinska University Hospital, Stockholm (Sweden); Bremell, Daniel; Hagberg, Lars [Department of Infectious Diseases, Institute of Biomedicine, Sahlgrenska Academy at the University of Gothenburg, Gothenburg (Sweden); Elam, Mikael [Department of Clinical Neuroscience and Rehabilitation, Insitute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg (Sweden); Blennow, Kaj [Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal (Sweden); Björk-Eriksson, Thomas [Department of Oncology, Institute of Clinical Sciences, Sahlgrenska Academy at the University of Gothenburg, Gothenburg (Sweden); Zetterberg, Henrik [Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal (Sweden); UCL Institute of Neurology, London (United Kingdom)

    2014-07-01

    Purpose: To examine whether cerebrospinal fluid biomarkers for neuroaxonal damage, neuroglial activation, and amyloid β–related processes could characterize the neurochemical response to cranial radiation. Methods and Materials: Before prophylactic cranial irradiation (PCI) of patients with small cell lung cancer, each patient underwent magnetic resonance imaging of the brain, lumbar puncture, and Mini-Mental State Examination of cognitive function. These examinations were repeated at approximately 3 and 12 months after radiation. Results: The major findings were as follows. (1) Cerebrospinal fluid markers for neuronal and neuroglial injury were elevated during the subacute phase after PCI. Neurofilament and T-tau increased 120% and 50%, respectively, after PCI (P<.05). The same was seen for the neuroglial markers YKL-40 and glial fibrillary acidic protein, which increased 144% and 106%, respectively, after PCI (P<.05). (2) The levels of secreted amyloid precursor protein-α and -β were reduced 44% and 46%, respectively, 3 months after PCI, and the levels continued to decrease as long as 1 year after treatment (P<.05). (3) Mini-Mental State Examination did not reveal any cognitive decline, indicating that a more sensitive test should be used in future studies. Conclusion: In conclusion, we were able to detect radiation therapy–induced changes in several markers reflecting neuronal injury, inflammatory/astroglial activation, and altered amyloid precursor protein/amyloid β metabolism, despite the low number of patients and quite moderate radiation doses (20-30 Gy). These changes are hypothesis generating and could potentially be used to assess the individual risk of developing long-term symptoms of chronic encephalopathy after PCI. This has to be evaluated in large studies with extended clinical follow-up and more detailed neurocognitive assessments.

  2. Caffeine triggers behavioral and neurochemical alterations in adolescent rats.

    Science.gov (United States)

    Ardais, A P; Borges, M F; Rocha, A S; Sallaberry, C; Cunha, R A; Porciúncula, L O

    2014-06-13

    Caffeine is the psychostimulant most consumed worldwide but concerns arise about the growing intake of caffeine-containing drinks by adolescents since the effects of caffeine on cognitive functions and neurochemical aspects of late brain maturation during adolescence are poorly known. We now studied the behavioral impact in adolescent male rats of regular caffeine intake at low (0.1mg/mL), moderate (0.3mg/mL) and moderate/high (1.0mg/mL) doses only during their active period (from 7:00 P.M. to 7:00 A.M.). All tested doses of caffeine were devoid of effects on locomotor activity, but triggered anxiogenic effects. Caffeine (0.3 and 1mg/mL) improved the performance in the object recognition task, but the higher dose of caffeine (1.0mg/mL) decreased the habituation to an open-field arena, suggesting impaired non-associative memory. All tested doses of caffeine decreased the density of glial fibrillary acidic protein and synaptosomal-associated protein-25, but failed to modify neuron-specific nuclear protein immunoreactivity in the hippocampus and cerebral cortex. Caffeine (0.3-1mg/mL) increased the density of brain-derived neurotrophic factor (BDNF) and proBDNF density as well as adenosine A1 receptor density in the hippocampus, whereas the higher dose of caffeine (1mg/mL) increased the density of proBDNF and BDNF and decreased A1 receptor density in the cerebral cortex. These findings document an impact of caffeine consumption in adolescent rats with a dual impact on anxiety and recognition memory, associated with changes in BDNF levels and decreases of astrocytic and nerve terminal markers without overt neuronal damage in hippocampal and cortical regions. Copyright © 2014 IBRO. Published by Elsevier Ltd. All rights reserved.

  3. WINCS Harmoni: Closed-loop dynamic neurochemical control of therapeutic interventions

    Science.gov (United States)

    Lee, Kendall H.; Lujan, J. Luis; Trevathan, James K.; Ross, Erika K.; Bartoletta, John J.; Park, Hyung Ook; Paek, Seungleal Brian; Nicolai, Evan N.; Lee, Jannifer H.; Min, Hoon-Ki; Kimble, Christopher J.; Blaha, Charles D.; Bennet, Kevin E.

    2017-04-01

    There has been significant progress in understanding the role of neurotransmitters in normal and pathologic brain function. However, preclinical trials aimed at improving therapeutic interventions do not take advantage of real-time in vivo neurochemical changes in dynamic brain processes such as disease progression and response to pharmacologic, cognitive, behavioral, and neuromodulation therapies. This is due in part to a lack of flexible research tools that allow in vivo measurement of the dynamic changes in brain chemistry. Here, we present a research platform, WINCS Harmoni, which can measure in vivo neurochemical activity simultaneously across multiple anatomical targets to study normal and pathologic brain function. In addition, WINCS Harmoni can provide real-time neurochemical feedback for closed-loop control of neurochemical levels via its synchronized stimulation and neurochemical sensing capabilities. We demonstrate these and other key features of this platform in non-human primate, swine, and rodent models of deep brain stimulation (DBS). Ultimately, systems like the one described here will improve our understanding of the dynamics of brain physiology in the context of neurologic disease and therapeutic interventions, which may lead to the development of precision medicine and personalized therapies for optimal therapeutic efficacy.

  4. Heavy Drinking in University Students With and Without Attention-Deficit/Hyperactivity Disorder: Contributions of Drinking Motives and Protective Behavioral Strategies

    Science.gov (United States)

    Howard, Andrea L; Pritchard, Tyler R

    2017-01-01

    This study examined rates of heavy drinking and alcohol problems in relation to drinking motives and protective behavioral strategies in university students with a documented current diagnosis of attention-deficit/hyperactivity disorder (ADHD; n = 31) compared with students with no history of ADHD (n = 146). Participants completed a Web-based questionnaire, and logistic regression models tested interactions between ADHD/comparison group membership and motives and protective strategies. Group differences in rates of heavy drinking and alcohol problems were not statistically significant, but medium-sized risk ratios showed that students without ADHD reported heavy drinking at a rate 1.44 times higher than students with ADHD and met screening criteria for problematic alcohol use at a rate of 1.54 times higher than students with ADHD. Other key findings were, first, that drinking to enhance positive affect (e.g., drinking because it is exciting), but not to cope with negative affect (e.g., drinking to forget your worries), predicted both heavy drinking and alcohol problems. Second, only protective behavioral strategies that emphasize alcohol avoidance predicted both heavy drinking and alcohol problems. Contrary to expectations, we found no ADHD-related moderation of effects of motives or protective strategies on our alcohol outcomes. Results of this study are limited by the small sample of students with ADHD but highlight tentative similarities and differences in effects of motives and strategies on drinking behaviors and alcohol problems reported by students with and without ADHD. PMID:28814878

  5. Anger-irritability as a mediator of attention deficit hyperactivity disorder risk for adolescent alcohol use and the contribution of coping skills.

    Science.gov (United States)

    Harty, Seth C; Gnagy, Elizabeth M; Pelham, William E; Molina, Brooke S G

    2017-05-01

    Research on susceptibility to alcohol use disorder within the attention deficit/hyperactivity disorder (ADHD) population has begun to expand examination of putative moderators and mediators in order to develop effective treatments. Specific dysregulated emotions have been separately associated with ADHD and with alcohol use difficulties. The current study is the first to conjointly study these variables by testing anger-irritability as a mediator of ADHD risk for adolescent alcohol use. Frequency of binge drinking, drunkenness, and alcohol problems were examined for 142 children with ADHD followed into adolescence and compared to 100 demographically similar youth without ADHD. Parent-rated anger-irritability was tested as a mediator. Behavioral and cognitive coping skills, which are key clinical treatment targets, were studied as moderators of these associations. Childhood ADHD was positively associated with anger-irritability and the drinking outcomes in adolescence. Anger-irritability mediated the association between ADHD and alcohol use problems, but not binge drinking or drunkenness. Behavioral and cognitive, but not avoidant, coping played a moderating role, but only of the association between childhood ADHD and anger-irritability. Active coping strategies by adolescents with ADHD may reduce the vulnerability to alcohol problems through a reduction of negative emotions. Future research on additional mediators and treatments that target these skills is encouraged. © 2016 Association for Child and Adolescent Mental Health.

  6. Deficits in comprehending wh-questions in children with hearing loss - the contribution of phonological short-term memory and syntactic complexity.

    Science.gov (United States)

    Penke, Martina; Wimmer, Eva

    2017-08-28

    The aim of the study is to investigate if German children with hearing loss (HL) display persisting problems in comprehending complex sentences and to find out whether these problems can be linked to limitations in phonological short-term memory (PSTM). A who-question comprehension test (picture pointing) and a nonword repetition (NWR) task were conducted with 21 German children with bilateral sensorineural HL (ages 3-4) and with age-matched 19 normal hearing (NH) children. Follow-up data (ages 6-8) are reported for 10 of the children with HL. The data reveal that the comprehension of who-questions as well as PSTM was significantly more impaired in children with HL than in children with NH. For both groups of participants, there were no correlations between question comprehension scores and performance in the NWR test. Syntactic complexity (subject vs. object question) affected question comprehension in children with HL, however, these problems were overcome at school age. In conclusion, the data indicate that a hearing loss affects the comprehension of complex sentences. The observed problems did, however, not persist and were, therefore, unlikely to be caused by a genuine syntactic deficit. For the tested wh-questions, there is no indication that syntactic comprehension problems of children with HL are due to limitations in PSTM.

  7. Heavy Drinking in University Students With and Without Attention-Deficit/Hyperactivity Disorder: Contributions of Drinking Motives and Protective Behavioral Strategies

    Directory of Open Access Journals (Sweden)

    Andrea L Howard

    2017-08-01

    Full Text Available This study examined rates of heavy drinking and alcohol problems in relation to drinking motives and protective behavioral strategies in university students with a documented current diagnosis of attention-deficit/hyperactivity disorder (ADHD; n = 31 compared with students with no history of ADHD (n = 146. Participants completed a Web-based questionnaire, and logistic regression models tested interactions between ADHD/comparison group membership and motives and protective strategies. Group differences in rates of heavy drinking and alcohol problems were not statistically significant, but medium-sized risk ratios showed that students without ADHD reported heavy drinking at a rate 1.44 times higher than students with ADHD and met screening criteria for problematic alcohol use at a rate of 1.54 times higher than students with ADHD. Other key findings were, first, that drinking to enhance positive affect (e.g., drinking because it is exciting, but not to cope with negative affect (e.g., drinking to forget your worries, predicted both heavy drinking and alcohol problems. Second, only protective behavioral strategies that emphasize alcohol avoidance predicted both heavy drinking and alcohol problems. Contrary to expectations, we found no ADHD-related moderation of effects of motives or protective strategies on our alcohol outcomes. Results of this study are limited by the small sample of students with ADHD but highlight tentative similarities and differences in effects of motives and strategies on drinking behaviors and alcohol problems reported by students with and without ADHD.

  8. Neurochemical dementia diagnostics for Alzheimer's disease and other dementias: an ISO 15189 perspective.

    Science.gov (United States)

    Waedt, Johanna; Kleinow, Martina; Kornhuber, Johannes; Lewczuk, Piotr

    2012-10-01

    Dementia is one of the most common causes of health problems in the elderly populations of Western industrialized countries. A combined analysis of cerebrospinal fluid-based neurochemical dementia diagnostics biomarkers (amyloid-β peptides, total tau and phosphorylated forms of tau) provides sensitivity and specificity in the range of 85% for the diagnosis of Alzheimer's disease, the most common cause of dementia. The alterations occur very early in the course of neurodegeneration, enabling medical follow-up of persons with increased risk of developing dementia. With a growing number of laboratories performing neurochemical dementia diagnostics routinely, it is important to standardize protocols and laboratory performance to enable comparisons of results and their interpretations. Together with the recently published expert guidelines for sample handling and preparation, as well as the interpretation (post-analytical) algorithms developed by experienced centers, ISO 15189 norm provides an extremely useful tool for standardization of neurochemical dementia diagnostics.

  9. Chronic neurochemical and behavioral changes in MPTP-lesioned C57BL/6 mice: a model for Parkinson's disease.

    Science.gov (United States)

    Sundström, E; Fredriksson, A; Archer, T

    1990-10-01

    The long-term effect of the parkinsonism inducing neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on pre- and postsynaptic structures of the nigrostriatal and mesolimbic dopamine (DA) system in adult C57BL/6 mice (2 x 40 mg/kg s.c.) was investigated using neurochemical and behavioral methods. It was found that MPTP induced a severe depletion of striatal DA levels (-80%) that persists for 4 weeks after treatment, with less severe effects in nucleus accumbens (-36%) and the olfactory tubercle (-52%). These depletions are associated with decreased tyrosine hydroxylase (TH) activity as determined in vivo and increased turnover of DA. MPTP treatment did not induce any change in the DA2-receptor as determined by [3H]spiperone binding or by two different behavioral tests, i.e. apomorphine-induced climbing and apomorphine-induced stereotypies. No significant weight loss during 4 weeks after MPTP was found. The spontaneous motor activity in these mice was profoundly and persistently depressed (-66%) as a result of the MPTP-induced DA denervation and the motor deficit was completely reversed by L-DOPA treatment. We suggest that MPTP-treated C57BL/6 mice may serve as a suitable model for Parkinson's disease.

  10. Dorsal and ventral stream contributions to form-from-motion perception in a patient with form-from motion deficit: a case report.

    Science.gov (United States)

    Mercier, Manuel R; Schwartz, Sophie; Spinelli, Laurent; Michel, Christoph M; Blanke, Olaf

    2017-03-01

    The main model of visual processing in primates proposes an anatomo-functional distinction between the dorsal stream, specialized in spatio-temporal information, and the ventral stream, processing essentially form information. However, these two pathways also communicate to share much visual information. These dorso-ventral interactions have been studied using form-from-motion (FfM) stimuli, revealing that FfM perception first activates dorsal regions (e.g., MT+/V5), followed by successive activations of ventral regions (e.g., LOC). However, relatively little is known about the implications of focal brain damage of visual areas on these dorso-ventral interactions. In the present case report, we investigated the dynamics of dorsal and ventral activations related to FfM perception (using topographical ERP analysis and electrical source imaging) in a patient suffering from a deficit in FfM perception due to right extrastriate brain damage in the ventral stream. Despite the patient's FfM impairment, both successful (observed for the highest level of FfM signal) and absent/failed FfM perception evoked the same temporal sequence of three processing states observed previously in healthy subjects. During the first period, brain source localization revealed cortical activations along the dorsal stream, currently associated with preserved elementary motion processing. During the latter two periods, the patterns of activity differed from normal subjects: activations were observed in the ventral stream (as reported for normal subjects), but also in the dorsal pathway, with the strongest and most sustained activity localized in the parieto-occipital regions. On the other hand, absent/failed FfM perception was characterized by weaker brain activity, restricted to the more lateral regions. This study shows that in the present case report, successful FfM perception, while following the same temporal sequence of processing steps as in normal subjects, evoked different patterns of

  11. Peptidergic nerve fibers in the urethra: Morphological and neurochemical characteristics in female mice of reproductive age.

    Science.gov (United States)

    Barry, Christine M; Ji, Esther; Sharma, Harman; Yap, Pauline; Spencer, Nicholas J; Matusica, Dusan; Haberberger, Rainer V

    2017-10-20

    Peptidergic nerve fibers provide important contributions to urethral function. Urethral innervation of female mice is not well documented. To determine the distribution and projection sites of nerve fibers immunoreactive for vasoactive intestinal peptide (VIP), calcitonin gene-related peptide (CGRP), substance P (SP), and neuropeptide Y (NPY) in the urethra of wild-type control mice and compare innervation characteristics between the proximal and distal urethra of young nullipara and older multipara mice. Furthermore, to identify the location and neurochemical coding of the spinal afferent nerve endings in the urethra, whose sensory neurons reside in lumbosacral dorsal root ganglia (DRG). Multiple labeling immunohistochemistry of urethral sections of nulliparous (6-8 weeks old), and multiparous (9-12 months old) mice, and anterograde axonal tracing from L5-S2 (DRG) in vivo. Abundant VIP-, CGRP-, SP-, and NPY-immunoreactive nerve fibers were identified in the adventitia, muscularis, and lamina propria of proximal and distal segments of the urethra. A proportion of fibers were closely associated with blood vessels, glands, and cells immunoreactive for PGP9.5. The epithelium contained abundant nerve fibers immunoreactive for CGRP and/or SP. Epithelial innervation was increased in the distal urethra of multipara mice. Abundant fibers were traced from L5-S2 DRG to all urethral regions. We present the first identification of spinal afferent endings in the urethra. Peptidergic nerve fibers, including multiple populations of spinal afferents, provide rich innervation of the female mouse urethra. The morphology of fibers in the epithelium and other regions suggests multiple nerve-cell interactions impacting on urethral function. © 2017 Wiley Periodicals, Inc.

  12. Behavioral and neurochemical characterization of new mouse model of hyperphenylalaninemia.

    Directory of Open Access Journals (Sweden)

    Tiziana Pascucci

    Full Text Available Hyperphenylalaninemia (HPA refers to all clinical conditions characterized by increased amounts of phenylalanine (PHE in blood and other tissues. According to their blood PHE concentrations under a free diet, hyperphenylalaninemic patients are commonly classified into phenotypic subtypes: classical phenylketonuria (PKU (PHE > 1200 µM/L, mild PKU (PHE 600-1200 µM/L and persistent HPA (PHE 120-600 µM/L (normal blood PHE < 120 µM/L. The current treatment for hyperphenylalaninemic patients is aimed to keep blood PHE levels within the safe range of 120-360 µM/L through a PHE-restricted diet, difficult to achieve. If untreated, classical PKU presents variable neurological and mental impairment. However, even mildly elevated blood PHE levels, due to a bad compliance to dietary treatment, produce cognitive deficits involving the prefrontal cortical areas, extremely sensible to PHE-induced disturbances. The development of animal models of different degrees of HPA is a useful tool for identifying the metabolic mechanisms underlying cognitive deficits induced by PHE. In this paper we analyzed the behavioral and biochemical phenotypes of different forms of HPA (control, mild-HPA, mild-PKU and classic-PKU, developed on the base of plasma PHE concentrations. Our results demonstrated that mice with different forms of HPA present different phenotypes, characterized by increasing severity of behavioral symptoms and brain aminergic deficits moving from mild HPA to classical PKU forms. In addition, our data identify preFrontal cortex and amygdala as the most affected brain areas and confirm the highest susceptibility of brain serotonin metabolism to mildly elevated blood PHE.

  13. Behavioral and Neurochemical Characterization of New Mouse Model of Hyperphenylalaninemia

    Science.gov (United States)

    Pascucci, Tiziana; Giacovazzo, Giacomo; Andolina, Diego; Accoto, Alessandra; Fiori, Elena; Ventura, Rossella; Orsini, Cristina; Conversi, David; Carducci, Claudia; Leuzzi, Vincenzo; Puglisi-Allegra, Stefano

    2013-01-01

    Hyperphenylalaninemia (HPA) refers to all clinical conditions characterized by increased amounts of phenylalanine (PHE) in blood and other tissues. According to their blood PHE concentrations under a free diet, hyperphenylalaninemic patients are commonly classified into phenotypic subtypes: classical phenylketonuria (PKU) (PHE > 1200 µM/L), mild PKU (PHE 600-1200 µM/L) and persistent HPA (PHE 120-600 µM/L) (normal blood PHE < 120 µM/L). The current treatment for hyperphenylalaninemic patients is aimed to keep blood PHE levels within the safe range of 120-360 µM/L through a PHE-restricted diet, difficult to achieve. If untreated, classical PKU presents variable neurological and mental impairment. However, even mildly elevated blood PHE levels, due to a bad compliance to dietary treatment, produce cognitive deficits involving the prefrontal cortical areas, extremely sensible to PHE-induced disturbances. The development of animal models of different degrees of HPA is a useful tool for identifying the metabolic mechanisms underlying cognitive deficits induced by PHE. In this paper we analyzed the behavioral and biochemical phenotypes of different forms of HPA (control, mild-HPA, mild-PKU and classic-PKU), developed on the base of plasma PHE concentrations. Our results demonstrated that mice with different forms of HPA present different phenotypes, characterized by increasing severity of behavioral symptoms and brain aminergic deficits moving from mild HPA to classical PKU forms. In addition, our data identify preFrontal cortex and amygdala as the most affected brain areas and confirm the highest susceptibility of brain serotonin metabolism to mildly elevated blood PHE. PMID:24376837

  14. Distinct Neurochemical Profiles of Spinocerebellar Ataxias 1, 2, 6, and Cerebellar Multiple System Atrophy

    Science.gov (United States)

    Öz, Gülin; Iltis, Isabelle; Hutter, Diane; Thomas, William; Bushara, Khalaf O.; Gomez, Christopher M.

    2011-01-01

    Hereditary and sporadic neurodegenerative ataxias are movement disorders that affect the cerebellum. Robust and objective biomarkers are critical for treatment trials of ataxias. In addition, such biomarkers may help discriminate between ataxia subtypes because these diseases display substantial overlap in clinical presentation and conventional MRI. Profiles of 10–13 neurochemical concentrations obtained in vivo by high field proton magnetic resonance spectroscopy (1H MRS) can potentially provide ataxia-type specific biomarkers. We compared cerebellar and brainstem neurochemical profiles measured at 4 T from 26 patients with spinocerebellar ataxias (SCA1, N=9; SCA2, N=7; SCA6, N=5) or cerebellar multiple system atrophy (MSA-C, N=5) and 15 age-matched healthy controls. The Scale for the Assessment and Rating of Ataxia (SARA) was used to assess disease severity. The patterns of neurochemical alterations relative to controls differed between ataxia types. Myo-inositol levels in the vermis, myo-inositol, total N-acetylaspartate, total creatine, glutamate, glutamine in the cerebellar hemispheres and myo-inositol, total N-acetylaspartate, glutamate in the pons were significantly different between patient groups (Bonferroni corrected pataxia types. Studies with higher numbers of patients and other ataxias are warranted to further investigate the clinical utility of neurochemical levels as measured by high-field MRS as ataxia biomarkers. PMID:20838948

  15. Development of intraoperative electrochemical detection: wireless instantaneous neurochemical concentration sensor for deep brain stimulation feedback.

    Science.gov (United States)

    Van Gompel, Jamie J; Chang, Su-Youne; Goerss, Stephan J; Kim, In Yong; Kimble, Christopher; Bennet, Kevin E; Lee, Kendall H

    2010-08-01

    Deep brain stimulation (DBS) is effective when there appears to be a distortion in the complex neurochemical circuitry of the brain. Currently, the mechanism of DBS is incompletely understood; however, it has been hypothesized that DBS evokes release of neurochemicals. Well-established chemical detection systems such as microdialysis and mass spectrometry are impractical if one is assessing changes that are happening on a second-to-second time scale or for chronically used implanted recordings, as would be required for DBS feedback. Electrochemical detection techniques such as fast-scan cyclic voltammetry (FSCV) and amperometry have until recently remained in the realm of basic science; however, it is enticing to apply these powerful recording technologies to clinical and translational applications. The Wireless Instantaneous Neurochemical Concentration Sensor (WINCS) currently is a research device designed for human use capable of in vivo FSCV and amperometry, sampling at subsecond time resolution. In this paper, the authors review recent advances in this electrochemical application to DBS technologies. The WINCS can detect dopamine, adenosine, and serotonin by FSCV. For example, FSCV is capable of detecting dopamine in the caudate evoked by stimulation of the subthalamic nucleus/substantia nigra in pig and rat models of DBS. It is further capable of detecting dopamine by amperometry and, when used with enzyme linked sensors, both glutamate and adenosine. In conclusion, WINCS is a highly versatile instrument that allows near real-time (millisecond) detection of neurochemicals important to DBS research. In the future, the neurochemical changes detected using WINCS may be important as surrogate markers for proper DBS placement as well as the sensor component for a "smart" DBS system with electrochemical feedback that allows automatic modulation of stimulation parameters. Current work is under way to establish WINCS use in humans.

  16. Prior methamphetamine self-administration attenuates the dopaminergic deficits caused by a subsequent methamphetamine exposure.

    Science.gov (United States)

    McFadden, Lisa M; Vieira-Brock, Paula L; Hanson, Glen R; Fleckenstein, Annette E

    2015-06-01

    Others and we have reported that prior methamphetamine (METH) exposure attenuates the persistent striatal dopaminergic deficits caused by a subsequent high-dose "binge" METH exposure. The current study investigated intermediate neurochemical changes that may contribute to, or serve to predict, this resistance. Rats self-administered METH or saline for 7 d. On the following day (specifically, 16 h after the conclusion of the final METH self-administration session), rats received a binge exposure of METH or saline (so as to assess the impact of prior METH self-administration), or were sacrificed without a subsequent METH exposure (i.e., to assess the status of the rats at what would have been the initiation of the binge METH treatment). Results revealed that METH self-administration per se decreased striatal dopamine (DA) transporter (DAT) function and DA content, as assessed 16 h after the last self-administration session. Exposure to a binge METH treatment beginning at this 16-h time point decreased DAT function and DA content as assessed 1 h after the binge METH exposure: this effect on DA content (but not DAT function) was attenuated if rats previously self-administered METH. In contrast, 24 h after the binge METH treatment prior METH self-administration: 1) attenuated deficits in DA content, DAT function and vesicular monoamine transporter-2 function; and 2) prevented increases in glial fibrillary acidic protein and DAT complex immunoreactivity. These data suggest that changes 24 h, but not 1 h, after binge METH exposure are predictive of tolerance against the persistence of neurotoxic changes following binge METH exposures. Copyright © 2015 Elsevier Ltd. All rights reserved.

  17. Behavioral, neurochemical and pharmaco-EEG profiles of the psychedelic drug 4-bromo-2,5-dimethoxyphenethylamine (2C-B) in rats.

    Science.gov (United States)

    Páleníček, Tomáš; Fujáková, Michaela; Brunovský, Martin; Horáček, Jiří; Gorman, Ingmar; Balíková, Marie; Rambousek, Lukáš; Syslová, Kamila; Kačer, Petr; Zach, Petr; Bubeníková-Valešová, Věra; Tylš, Filip; Kubešová, Anna; Puskarčíková, Jana; Höschl, Cyril

    2013-01-01

    Behavioral, neurochemical and pharmaco-EEG profiles of a new synthetic drug 4-bromo-2,5-dimethoxyphenethylamine (2C-B) in rats were examined. Locomotor effects, prepulse inhibition (PPI) of acoustic startle reaction (ASR), dopamine and its metabolite levels in nucleus accumbens (NAc), EEG power spectra and coherence in freely moving rats were analysed. Amphetamine was used as a reference compound. 2C-B had a biphasic effect on locomotion with initial inhibitory followed by excitatory effect; amphetamine induced only hyperlocomotion. Both drugs induced deficits in the PPI; however they had opposite effects on ASR. 2C-B increased dopamine but decreased 3,4-dihydroxyphenylacetic acid (DOPAC) in the NAc. Low doses of 2C-B induced a decrease in EEG power spectra and coherence. On the contrary, high dose of 2C-B 50 mg/kg had a temporally biphasic effect with an initial decrease followed by an increase in EEG power; decrease as well as increase in EEG coherence was observed. Amphetamine mainly induced an increase in EEG power and coherence in theta and alpha bands. Increases in the theta and alpha power and coherence in 2C-B and amphetamine were temporally linked to an increase in locomotor activity and DA levels in NAc. 2C-B is a centrally active compound similar to other hallucinogens, entactogens and stimulants. Increased dopamine and decreased DOPAC in the NAc may reflect its psychotomimetic and addictive potential and monoaminoxidase inhibition. Alterations in brain functional connectivity reflected the behavioral and neurochemical changes produced by the drug; a correlation between EEG changes and locomotor behavior was observed.

  18. Dysregulation of brain reward systems in eating disorders: neurochemical information from animal models of binge eating, bulimia nervosa, and anorexia nervosa.

    Science.gov (United States)

    Avena, Nicole M; Bocarsly, Miriam E

    2012-07-01

    Food intake is mediated, in part, through brain pathways for motivation and reinforcement. Dysregulation of these pathways may underlay some of the behaviors exhibited by patients with eating disorders. Research using animal models of eating disorders has greatly contributed to the detailed study of potential brain mechanisms that many underlie the causes or consequences of aberrant eating behaviors. This review focuses on neurochemical evidence of reward-related brain dysfunctions obtained through animal models of binge eating, bulimia nervosa, or anorexia nervosa. The findings suggest that alterations in dopamine (DA), acetylcholine (ACh) and opioid systems in reward-related brain areas occur in response to binge eating of palatable foods. Moreover, animal models of bulimia nervosa suggest that while bingeing on palatable food releases DA, purging attenuates the release of ACh that might otherwise signal satiety. Animal models of anorexia nervosa suggest that restricted access to food enhances the reinforcing effects of DA when the animal does eat. The activity-based anorexia model suggests alterations in mesolimbic DA and serotonin occur as a result of restricted eating coupled with excessive wheel running. These findings with animal models complement data obtained through neuroimaging and pharmacotherapy studies of clinical populations. Information on the neurochemical consequences of the behaviors associated with these eating disorders will be useful in understanding these complex disorders and may inform future therapeutic approaches, as discussed here. This article is part of a Special Issue entitled 'Central Control of Food Intake'. Copyright © 2011 Elsevier Ltd. All rights reserved.

  19. Longitudinal neurochemical modifications in the aging mouse brain measured in vivo by 1H magnetic resonance spectroscopy.

    Science.gov (United States)

    Duarte, João M N; Do, Kim Q; Gruetter, Rolf

    2014-07-01

    Alterations to brain homeostasis during development are reflected in the neurochemical profile determined noninvasively by (1)H magnetic resonance spectroscopy. We determined longitudinal biochemical modifications in the cortex, hippocampus, and striatum of C57BL/6 mice aged between 3 and 24 months . The regional neurochemical profile evolution indicated that aging induces general modifications of neurotransmission processes (reduced GABA and glutamate), primary energy metabolism (altered glucose, alanine, and lactate) and turnover of lipid membranes (modification of choline-containing compounds and phosphorylethanolamine), which are all probably involved in the frequently observed age-related cognitive decline. Interestingly, the neurochemical profile was different in male and female mice, particularly in the levels of taurine that may be under the control of estrogen receptors. These neurochemical profiles constitute the basal concentrations in cortex, hippocampus, and striatum of healthy aging male and female mice. Copyright © 2014 Elsevier Inc. All rights reserved.

  20. Integrative pathways linking close family ties to health: A neurochemical perspective.

    Science.gov (United States)

    Uchino, Bert N; Way, Baldwin M

    2017-09-01

    The quality of one's familial life, for better or worse, has been linked to physical health. Such associations are evident across a number of acute and chronic conditions and highlight the widespread impact that close relationships have on physical health. However, the field currently lacks a complete understanding of the integrative biological pathways underlying the association between close relationships and disease risk. This article reviews the main peripheral biological and central nervous system pathways linking positive and negative familial relationship processes to physical health outcomes. It emphasizes the role of neurochemical pathways in mediating the influence of social relationships on health-relevant peripheral physiological systems using the oxytocin system as a model. Such neurochemical approaches are an important step toward a more integrative understanding of complex biological pathways and has novel theoretical and intervention implications. (PsycINFO Database Record (c) 2017 APA, all rights reserved).

  1. Behavioral Deficits Are Accompanied by Immunological and Neurochemical Changes in a Mouse Model for Neuropsychiatric Lupus (NP-SLE)

    DEFF Research Database (Denmark)

    Li, Yan; Eskelund, Amanda; Zhou, H

    2015-01-01

    Neuropsychiatric symptoms of systemic lupus erythematosus (NP-SLE) have been understudied compared to end-organ failure and peripheral pathology. Neuropsychiatric symptoms, particularly affective and cognitive indications, may be among the earliest manifestations of SLE. Among the potential...... pathophysiological mechanisms responsible for NP-SLE are increased peripheral pro-inflammatory cytokines, subsequent induction of indoleamine-2,3-dioxygenase (IDO) and activation of the kynurenine pathway. In the MRL/MpJ-Faslpr (MRL/lpr) murine model of lupus, depression-like behavior and cognitive dysfunction...... is evident before significant levels of autoantibody titers and nephritis are present. We examined the behavioral profile of MRL/lpr mice and their congenic controls, a comprehensive plasma cytokine and chemokine profile, and brain levels of serotonin and kynurenine pathway metabolites. Consistent...

  2. Behavioral Deficits Are Accompanied by Immunological and Neurochemical Changes in a Mouse Model for Neuropsychiatric Lupus (NP-SLE

    Directory of Open Access Journals (Sweden)

    Yan Li

    2015-07-01

    Full Text Available Neuropsychiatric symptoms of systemic lupus erythematosus (NP-SLE have been understudied compared to end-organ failure and peripheral pathology. Neuropsychiatric symptoms, particularly affective and cognitive indications, may be among the earliest manifestations of SLE. Among the potential pathophysiological mechanisms responsible for NP-SLE are increased peripheral pro-inflammatory cytokines, subsequent induction of indoleamine-2,3-dioxygenase (IDO and activation of the kynurenine pathway. In the MRL/MpJ-Faslpr (MRL/lpr murine model of lupus, depression-like behavior and cognitive dysfunction is evident before significant levels of autoantibody titers and nephritis are present. We examined the behavioral profile of MRL/lpr mice and their congenic controls, a comprehensive plasma cytokine and chemokine profile, and brain levels of serotonin and kynurenine pathway metabolites. Consistent with previous studies, MRL/lpr mice had increased depression-like behavior and visuospatial memory impairment. Plasma levels of different inflammatory molecules (Haptoglobin, interleukin 10 (IL-10, interferon γ-inducible protein 10 (IP-10/CXCL10, lymphotactin, macrophage inhibitory protein 3β (MIP-3β/CCL19, monocyte chemotactic protein 1, 3 and 5 (MCP-1/CCL2, MCP-3/CCL7, MCP-5/CCL12, vascular cell adhesion molecule 1 (VCAM-1, lymphotactin and interferon γ (IFN-γ were increased in MRL/lpr mice. In cortex and hippocampus, MRL/lpr mice had increased levels of kynurenine pathway metabolites (kynurenine, 3-hydroxykynurenine, 3-hydroxynthranilic acid and quinolinic acid. Therefore, our study suggests that increased cytokine expression may be critical in the regulation subtle aspects of brain function in NP-SLE via induction of IDO and tryptophan/kynurenine metabolism.

  3. Immunostaining of Biocytin-filled and Processed Sections for Neurochemical Markers.

    Science.gov (United States)

    Swietek, Bogumila; Gupta, Akshay; Proddutur, Archana; Santhakumar, Vijayalakshmi

    2016-12-31

    Electrophysiological recordings of cells using the patch clamp technique have allowed for the identification of different neuronal types based on firing patterns. The inclusion of biocytin/neurobiotin in the recording electrode permits post-hoc recovery of morphological details, which are necessary to determine the dendritic arborization and the regions targeted by the axons of the recorded neurons. However, given the presence of morphologically similar neurons with distinct neurochemical identities and functions, immunohistochemical staining for cell-type-specific proteins is essential to definitively identify neurons. To maintain network connectivity, brain sections for physiological recordings are prepared at a thickness of 300 µm or greater. However, this thickness often hinders immunohistological postprocessing due to issues with antibody penetration, necessitating the resectioning of the tissue. Resectioning of slices is a challenging art, often resulting in the loss of tissue and morphology of the cells from which electrophysiological data was obtained, rendering the data unusable. Since recovery of morphology would limit data loss and guide in the selection of neuronal markers, we have adopted a strategy of recovering cell morphology first, followed by secondary immunostaining. We introduce a practical approach to biocytin filling during physiological recordings and subsequent serial immunostaining for the recovery of morphology, followed by the restaining of sections to determine the neurochemical identity. We report that sections that were filled with biocytin, fixed with paraformaldehyde (PFA), stained, and coverslipped can be removed and restained with a second primary antibody days later. This restaining involves the removal of the coverslip, the washing of sections in a buffer solution, and the incubation of primary and secondary antibodies to reveal the neurochemical identity. The method is advantageous for eliminating data loss due to an inability

  4. Induction of gram-negative bacterial growth by neurochemical containing banana (Musa x paradisiaca) extracts.

    Science.gov (United States)

    Lyte, M

    1997-09-15

    Bananas contain large quantities of neurochemicals. Extracts from the peel and pulp of bananas in increasing stages of ripening were prepared and evaluated for their ability to modulate the growth of non-pathogenic and pathogenic bacteria. Extracts from the peel, and to a much lesser degree the pulp, increased the growth of Gram-negative bacterial strains Escherichia coli O157:H7, Shigella flexneri, Enterobacter cloacae and Salmonella typhimurium, as well as two non-pathogenic E. coli strains, in direct relation to the content of norepinephrine and dopamine, but not serotonin. The growth of Gram-positive bacteria was not altered by any of the extracts. Supplementation of vehicle and pulp cultures with norepinephrine or dopamine yielded growth equivalent to peel cultures. Total organic analysis of extracts further demonstrated that the differential effects of peel and pulp on bacterial growth was not nutritionally based, but due to norepinephrine and dopamine. These results suggest that neurochemicals contained within foodstuffs may influence the growth of pathogenic and indigenous bacteria through direct neurochemical-bacterial interactions.

  5. In vivo magnetic resonance studies reveal neuroanatomical and neurochemical abnormalities in the serine racemase knockout mouse model of schizophrenia.

    Science.gov (United States)

    Puhl, Matthew D; Mintzopoulos, Dionyssios; Jensen, J Eric; Gillis, Timothy E; Konopaske, Glenn T; Kaufman, Marc J; Coyle, Joseph T

    2015-01-01

    Decreased availability of the N-methyl-D-aspartate receptor (NMDAR) co-agonist D-serine is thought to promote NMDAR hypofunction and contribute to the pathophysiology of schizophrenia, including neuroanatomical abnormalities, such as cortical atrophy and ventricular enlargement, and neurochemical abnormalities, such as aberrant glutamate and γ-aminobutyric acid (GABA) signaling. It is thought that these abnormalities directly relate to the negative symptoms and cognitive impairments that are hallmarks of the disorder. Because of the genetic complexity of schizophrenia, animal models of the disorder are extremely valuable for the study of genetically predisposing factors. Our laboratory developed a transgenic mouse model lacking serine racemase (SR), the synthetic enzyme of d-serine, polymorphisms of which are associated with schizophrenia. Null mutants (SR-/-) exhibit NMDAR hypofunction and cognitive impairments. We used 9.4 T magnetic resonance imaging (MRI) and proton spectroscopy (MRS) to compare in vivo brain structure and neurochemistry in wildtype (WT) and SR-/- mice. Mice were anesthetized with isoflurane for MRI and MRS scans. Compared to WT controls, SR-/- mice exhibited 23% larger ventricular volumes (pcomparable to those previously reported in humans with schizophrenia. Copyright © 2015 Elsevier Inc. All rights reserved.

  6. Neural and neurochemical basis of reinforcement-guided decision making.

    Science.gov (United States)

    Khani, Abbas; Rainer, Gregor

    2016-08-01

    Decision making is an adaptive behavior that takes into account several internal and external input variables and leads to the choice of a course of action over other available and often competing alternatives. While it has been studied in diverse fields ranging from mathematics, economics, ecology, and ethology to psychology and neuroscience, recent cross talk among perspectives from different fields has yielded novel descriptions of decision processes. Reinforcement-guided decision making models are based on economic and reinforcement learning theories, and their focus is on the maximization of acquired benefit over a defined period of time. Studies based on reinforcement-guided decision making have implicated a large network of neural circuits across the brain. This network includes a wide range of cortical (e.g., orbitofrontal cortex and anterior cingulate cortex) and subcortical (e.g., nucleus accumbens and subthalamic nucleus) brain areas and uses several neurotransmitter systems (e.g., dopaminergic and serotonergic systems) to communicate and process decision-related information. This review discusses distinct as well as overlapping contributions of these networks and neurotransmitter systems to the processing of decision making. We end the review by touching on neural circuitry and neuromodulatory regulation of exploratory decision making. Copyright © 2016 the American Physiological Society.

  7. Multiple Deficits in ADHD: Executive Dysfunction, Delay Aversion, Reaction Time Variability, and Emotional Deficits

    Science.gov (United States)

    Sjowall, Douglas; Roth, Linda; Lindqvist, Sofia; Thorell, Lisa B.

    2013-01-01

    Background: The notion that ADHD constitutes a heterogeneous disorder is well accepted. However, this study contributes with new important knowledge by examining independent effects of a large range of neuropsychological deficits. In addition, the study investigated whether deficits in emotional functioning constitute a dissociable component of…

  8. Mercury Vapour Long-Lasting Exposure: Lymphocyte Muscarinic Receptors as Neurochemical Markers of Accidental Intoxication

    Directory of Open Access Journals (Sweden)

    E. Roda

    2016-01-01

    Full Text Available Introduction. Chronic poisoning may result in home setting after mercury (Hg vapours inhalation from damaged devices. We report a chronic, nonoccupational Hg poisoning due to 10-year indoor exposure to mercury spillage. Case Report. A 72-year-old man with polyneuropathy of suspected toxic origin. At hospitalization, toxicological clinical evaluations confirmed the altered neurological picture documented across the last decade. Periodic blood and urine Hg levels (BHg, UHg monitoring were performed from admission (t0, until 1 year later (t2, paralleled by blood neurochemical markers assessment, that is, lymphocytes muscarinic receptors (l-MRs. At t0: BHg and UHg were 27 and 1.4 microg/L, respectively (normal values: BHg 1–4.5; UHg 0.1–4.5, associated with l-MRs increase, 185.82 femtomoL/million lymphocytes (normal range: 8.0–16.0. At t1 (two days after DMSA-mobilization test, BHg weak reduction, paralleled by UHg 3.7-fold increase, was measured together with further l-MRs enhancement (205.43 femtomoL/million lymphocytes. At t2 (eight months after two cycles of DMSA chelating therapy ending, gradual improving of clinical manifestations was accompanied by progressive decrease of BHg and UHg (4.0 and 2.8 microg/L, resp. and peripheral l-MRs neurochemical marker (24.89 femtomoL/million lymphocytes. Conclusion. l-MRs modulatory effect supports their use as peripheral neurochemical marker in Hg poisoning diagnosis and chelation therapy monitoring.

  9. Mercury Vapour Long-Lasting Exposure: Lymphocyte Muscarinic Receptors as Neurochemical Markers of Accidental Intoxication.

    Science.gov (United States)

    Roda, E; Giampreti, A; Vecchio, S; Apostoli, P; Coccini, T

    2016-01-01

    Introduction. Chronic poisoning may result in home setting after mercury (Hg) vapours inhalation from damaged devices. We report a chronic, nonoccupational Hg poisoning due to 10-year indoor exposure to mercury spillage. Case Report. A 72-year-old man with polyneuropathy of suspected toxic origin. At hospitalization, toxicological clinical evaluations confirmed the altered neurological picture documented across the last decade. Periodic blood and urine Hg levels (BHg, UHg) monitoring were performed from admission (t0), until 1 year later (t2), paralleled by blood neurochemical markers assessment, that is, lymphocytes muscarinic receptors (l-MRs). At t0: BHg and UHg were 27 and 1.4 microg/L, respectively (normal values: BHg 1-4.5; UHg 0.1-4.5), associated with l-MRs increase, 185.82 femtomoL/million lymphocytes (normal range: 8.0-16.0). At t1 (two days after DMSA-mobilization test), BHg weak reduction, paralleled by UHg 3.7-fold increase, was measured together with further l-MRs enhancement (205.43 femtomoL/million lymphocytes). At t2 (eight months after two cycles of DMSA chelating therapy ending), gradual improving of clinical manifestations was accompanied by progressive decrease of BHg and UHg (4.0 and 2.8 microg/L, resp.) and peripheral l-MRs neurochemical marker (24.89 femtomoL/million lymphocytes). Conclusion. l-MRs modulatory effect supports their use as peripheral neurochemical marker in Hg poisoning diagnosis and chelation therapy monitoring.

  10. Cannabinoids for the Treatment of Schizophrenia? A Balanced Neurochemical Framework for Both Adverse and Therapeutic Effects of Cannabis Use

    Directory of Open Access Journals (Sweden)

    Carissa M. Coulston

    2011-01-01

    Full Text Available Recent studies have found that cannabinoids may improve neuropsychological performance, ameliorate negative symptoms, and have antipsychotic properties for a subgroup of the schizophrenia population. These findings are in contrast to the longstanding history of adverse consequences of cannabis use, predominantly on the positive symptoms, and a balanced neurochemical basis for these opposing views is lacking. This paper details a review of the neurobiological substrates of schizophrenia and the neurochemical effects of cannabis use in the normal population, in both cortical (in particular prefrontal and subcortical brain regions. The aim of this paper is to provide a holistic neurochemical framework in which to understand how cannabinoids may impair, or indeed, serve to ameliorate the positive and negative symptoms as well as cognitive impairment. Directions in which future research can proceed to resolve the discrepancies are briefly discussed.

  11. Attention deficit-hyperactivity disorder and early-onset bipolar disorder: two facets of one entity?

    Science.gov (United States)

    Zepf, Florian D

    2009-01-01

    Early-onset bipolar disorder (BD) and attention-deficit-hyperactivity disorder (ADHD) have recently been the subject of highly controversial debate, due to theories regarding underlying pathophysiological processes and a clinical overlap of symptoms. Epidemiological data, clinical aspects neuroimaging, neurochemical, and genetic studies suggest that there may be a possible relationship between biological factors and clinical characteristics in the development of symptoms. However, longitudinal data supporting the hypothesis of a diagnostic shift from BD to ADHD symptoms and vice versa are currently not available. These would be essential to enable further investigations into whether these two disorders possibly represent two different aspects of an underlying common psychopathophysiological entity.

  12. Microdialysis Coupled with LC-MS/MS for In Vivo Neurochemical Monitoring.

    Science.gov (United States)

    Zestos, Alexander G; Kennedy, Robert T

    2017-09-01

    Microdialysis is a powerful sampling technique used to monitor small molecules in vivo. Despite the many applications of microdialysis sampling, it is limited by the method of analyzing the resulting samples. An emerging technique for analysis of microdialysis samples is liquid chromatography-tandem mass spectrometry (LC-MS/MS). This technique is highly versatile, allowing multiplexed analysis of neurotransmitters, metabolites, and neuropeptides. Using LC-MS/MS for polar neurotransmitters is hampered by weak retention reverse phase LC columns. Several derivatization reagents have been utilized to enhance separation and resolution of neurochemicals in dialysate samples including benzoyl chloride (BzCl), dansyl chloride, formaldehyde, ethylchloroformate, and propionic anhydride. BzCl reacts with amine and phenol groups so that many neurotransmitters can be labeled. Besides improving separation on reverse phase columns, this reagent also increases sensitivity. It is available in a heavy form so that it can be used to make stable-isotope labeled internal standard for improved quantification. Using BzCl with LC-MS/MS has allowed for measuring as many as 70 neurochemicals in a single assay. With slightly different conditions, LC-MS/MS has also been used for monitoring endocannabinoids. LC-MS/MS is also useful for neuropeptide assay because it allows for highly sensitive, sequence specific measurement of most peptides. These advances have allowed for multiplexed neurotransmitter measurements in behavioral, circuit analysis, and drug effect studies.

  13. No neurochemical evidence of brain injury after blast overpressure by repeated explosions or firing heavy weapons.

    Science.gov (United States)

    Blennow, K; Jonsson, M; Andreasen, N; Rosengren, L; Wallin, A; Hellström, P A; Zetterberg, H

    2011-04-01

    Psychiatric and neurological symptoms are common among soldiers exposed to blast without suffering a direct head injury. It is not known whether such symptoms are direct consequences of blast overpressure. To examine if repeated detonating explosions or firing if of heavy weapons is associated with neurochemical evidence of brain damage. Three controlled experimental studies. In the first, army officers were exposed to repeated firing of a FH77B howitzer or a bazooka. Cerebrospinal fluid (CSF) was taken post-exposure to measure biomarkers for brain damage. In the second, officers were exposed for up to 150 blasts by firing a bazooka, and in the third to 100 charges of detonating explosives of 180 dB. Serial serum samples were taken after exposure. Results were compared with a control group consisting of 19 unexposed age-matched healthy volunteers. The CSF biomarkers for neuronal/axonal damage (tau and neurofilament protein), glial cell injury (GFAP and S-100b), blood-brain barrier damage (CSF/serum albumin ratio) and hemorrhages (hemoglobin and bilirubin) and the serum GFAP and S-100b showed normal and stable levels in all exposed officers. Repeated exposure to high-impact blast does not result in any neurochemical evidence of brain damage. These findings are of importance for soldiers regularly exposed to high-impact blast when firing artillery shells or other types of heavy weapons. © 2010 John Wiley & Sons A/S.

  14. Neurochemical effects of extended exposure to white spirit vapour at three concentration levels.

    Science.gov (United States)

    Savolainen, H; Pfäffli, P

    1982-03-01

    Male Wistar rats were exposed to 575 (100 ppm), 2875 (500 ppm) or 5750 mg/m3 (1000 ppm) white spirit vapour for 4-17 weeks 5 days a week, 6 h daily. Perirenal fat solvent concentration corresponded in composition and concentration to those of the vapour at all times. The neurochemical effects included a dose-dependent decrease in the cerebellar succinate dehydrogenase activity for 8 weeks while creatine kinase activity increased after 12 weeks. The specific creatine kinase activity in the glial cell fraction, a marker for astroglia, did not increase suggesting proliferation of astroglial cells in the homogenate. The serum creatine kinase activity originating mainly from striated muscle was below the control range at the two higher concentrations after 12 weeks. Simultaneous analyses for isolated muscle membrane sialic acid and uronic acid residues showed decreased concentrations in proportion to lipid phosphorus or total membrane protein. Thus, the white spirit mixture has neurochemical effects possibly caused by paraffins and the same components may have caused the muscle cell membrane effects. The lowest exposure concentration represents a virtual 'no effect' level for rats in the 17-week exposure.

  15. The trace amine-associated receptor 1 modulates methamphetamine's neurochemical and behavioral effects.

    Science.gov (United States)

    Cotter, Rachel; Pei, Yue; Mus, Liudmila; Harmeier, Anja; Gainetdinov, Raul R; Hoener, Marius C; Canales, Juan J

    2015-01-01

    The newly discovered trace amine-associated receptor 1 (TAAR1) has the ability to regulate both dopamine function and psychostimulant action. Here, we tested in rats the ability of RO5203648, a selective TAAR1 partial agonist, to modulate the physiological and behavioral effects of methamphetamine (METH). In experiment 1, RO5203468 dose- and time-dependently altered METH-induced locomotor activity, manifested as an early attenuation followed by a late potentiation of METH's stimulating effects. In experiment 2, rats received a 14-day treatment regimen during which RO5203648 was co-administered with METH. RO5203648 dose-dependently attenuated METH-stimulated hyperactivity, with the effects becoming more apparent as the treatments progressed. After chronic exposure and 3-day withdrawal, rats were tested for locomotor sensitization. RO5203648 administration during the sensitizing phase prevented the development of METH sensitization. However, RO5203648, at the high dose, cross-sensitized with METH. In experiment 3, RO5203648 dose-dependently blocked METH self-administration without affecting operant responding maintained by sucrose, and exhibited lack of reinforcing efficacy when tested as a METH's substitute. Neurochemical data showed that RO5203648 did not affect METH-mediated DA efflux and uptake inhibition in striatal synaptosomes. In vivo, however, RO5203648 was able to transiently inhibit METH-induced accumulation of extracellular DA levels in the nucleus accumbens. Taken together, these data highlight the significant potential of TAAR1 to modulate METH's neurochemical and behavioral effects.

  16. Modulatory effect of cilostazol on tramadol-induced behavioral and neurochemical alterations in rats challenged across the forced swim despair test

    Directory of Open Access Journals (Sweden)

    Noha M. Gamil

    2016-06-01

    Full Text Available Pain-associated depression is encountered clinically in some cases such as cancer, chronic neuropathy, and after operations. Tramadol is an opioid analgesic drug that may modulate monoaminergic neurotransmission by inhibition of noradrenaline and serotonin reuptake that may contribute to its antidepressant-like effects. Clinically, tramadol is used either alone or in combination with other NSAIDs in the treatment of cases associated with pain and depression, e.g. low back pain, spinal cord injury, and post-operative pain management. However, tramadol monotherapy as an antidepressant is impeded by severe adverse effects including seizures and serotonin syndrome. Interestingly, phosphodiesterase-III inhibitors demonstrated novel promising antidepressant effects. Among which, cilostazol was reported to attenuate depression in post-stroke cases, geriatrics and patients undergoing carotid artery stenting. Therefore, this study was carried out to investigate the possible antidepressant-like effects of tramadol and/or cilostazol on the behavioral level in experimental animals, and to examine the neurochemical and biochemical effects of tramadol, cilostazol and their combination in rats, in order to explore the probable mechanisms of action underlying their effects. To achieve our target, male albino mice and rats were randomly allocated into five groups and administered either vehicle for control, fluoxetine (20 mg/kg, p.o., tramadol HCl (20 mg/kg, p.o., cilostazol (100 mg/kg, p.o., or combination of both tramadol and cilostazol. At day 14, mice and rats were challenged in the tail suspension test and forced swim test, respectively. Rats were sacrificed and brains were isolated for determination of brain monoamines, MDA, NO, SOD, and TNF-α. The current results showed that concurrent administration of cilostazol to tramadol-treated animals modulated depression on the behavioral level, and showed ameliorative neurochemical and biochemical effects

  17. Emotion and mood adaptations in the peripartum female:complementary contributions of GABA and oxytocin.

    Science.gov (United States)

    Lonstein, J S; Maguire, J; Meinlschmidt, G; Neumann, I D

    2014-10-01

    Peripartum hormones and sensory cues from young modify the maternal brain in ways that can render females either at risk for, or resilient to, elevated anxiety and depression. The neurochemical systems underlying these aspects of maternal emotional and mood states include the inhibitory neurotransmitter GABA and the neuropeptide oxytocin (OXT). Data from laboratory rodents indicate that increased activity at the GABA(A) receptor contributes to the postpartum suppression of anxiety-related behaviour that is mediated by physical contact with offspring, whereas dysregulation in GABAergic signalling results in deficits in maternal care, as well as anxiety- and depression-like behaviours during the postpartum period. Similarly, activation of the brain OXT system accompanied by increased OXT release within numerous brain sites in response to reproductive stimuli also reduces postpartum anxiety- and depression-like behaviours. Studies of peripartum women are consistent with these findings in rodents. Given the similar consequences of elevated central GABA and OXT activity on maternal anxiety and depression, balanced and partly reciprocal interactions between these two systems may be essential for their effects on maternal emotional and mood states, in addition to other aspects of postpartum behaviour and physiology. © 2014 British Society for Neuroendocrinology.

  18. Effects of Gladiolus dalenii on the Stress-Induced Behavioral, Neurochemical, and Reproductive Changes in Rats

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    David Fotsing

    2017-09-01

    Full Text Available Gladiolus dalenii is a plant commonly used in many regions of Cameroon as a cure for various diseases like headaches, epilepsy, schizophrenia, and mood disorders. Recent studies have revealed that the aqueous extract of G. dalenii (AEGD exhibited antidepressant-like properties in rats. Therefore, we hypothesized that the AEGD could protect from the stress-induced behavioral, neurochemical, and reproductive changes in rats. The objective of the present study was to elucidate the effect of the AEGD on behavioral, neurochemical, and reproductive characteristics, using female rats subjected to chronic immobilization stress. The chronic immobilization stress (3 h per day for 28 days was applied to induce female reproductive and behavioral impairments in rats. The immobilization stress was provoked in rats by putting them separately inside cylindrical restrainers with ventilated doors at ambient temperature. The plant extract was given to rats orally everyday during 28 days, 5 min before induction of stress. On a daily basis, a vaginal smear was made to assess the duration of the different phases of the estrous cycle and at the end of the 28 days of chronic immobilization stress, the rat’s behavior was assessed in the elevated plus maze. They were sacrificed by cervical disruption. The organs were weighed, the ovary histology done, and the biochemical parameters assessed. The findings of this research revealed that G. dalenii increased the entries and the time of open arm exploration in the elevated plus maze. Evaluation of the biochemical parameters levels indicated that there was a significant reduction in the corticosterone, progesterone, and prolactin levels in the G. dalenii aqueous extract treated rats compared to stressed rats whereas the levels of serotonin, triglycerides, adrenaline, cholesterol, glucose estradiol, follicle stimulating hormone and luteinizing hormone were significantly increased in the stressed rats treated with, G. dalenii

  19. Cerebellar neurochemical alterations in spinocerebellar ataxia type 14 appear to include glutathione deficiency.

    Science.gov (United States)

    Doss, Sarah; Rinnenthal, Jan Leo; Schmitz-Hübsch, Tanja; Brandt, Alexander U; Papazoglou, Sebastian; Lux, Silke; Maul, Stephan; Würfel, Jens; Endres, Matthias; Klockgether, Thomas; Minnerop, Martina; Paul, Friedemann

    2015-08-01

    Autosomal dominant ataxia type 14 (SCA14) is a rare usually adult-onset progressive disorder with cerebellar neurodegeneration caused by mutations in protein kinase C gamma. We set out to examine cerebellar and extracerebellar neurochemical changes in SCA14 by MR spectroscopy. In 13 SCA14 patients and 13 healthy sex- and age-matched controls, 3-T single-voxel brain proton MR spectroscopy was performed in a cerebellar voxel of interest (VOI) at TE = 30 ms to obtain a neurochemical profile of metabolites with short relaxation times. In the cerebellum and in additional VOIs in the prefrontal cortex, motor cortex, and somatosensory cortex, a second measurement was performed at TE = 144 ms to mainly extract the total N-acetyl-aspartate (tNAA) signal besides the signals for total creatine (tCr) and total choline (tCho). The cerebellar neurochemical profile revealed a decrease in glutathione (6.12E-06 ± 2.50E-06 versus 8.91E-06 ± 3.03E-06; p = 0028) and tNAA (3.78E-05 ± 5.67E-06 versus 4.25E-05 ± 5.15E-06; p = 0023) and a trend for reduced glutamate (2.63E-05 ± 6.48E-06 versus 3.15E-05 ± 7.61E-06; p = 0062) in SCA14 compared to controls. In the tNAA-focused measurement, cerebellar tNAA (296.6 ± 42.6 versus 351.7 ± 16.5; p = 0004) and tCr (272.1 ± 25.2 versus 303.2 ± 31.4; p = 0004) were reduced, while the prefrontal, somatosensory and motor cortex remained unaffected compared to controls. Neuronal pathology in SCA14 detected by MR spectroscopy was restricted to the cerebellum and did not comprise cortical regions. In the cerebellum, we found in addition to signs of neurodegeneration a glutathione reduction, which has been associated with cellular damage by oxidative stress in other neurodegenerative diseases such as Parkinson's disease and Friedreich's ataxia.

  20. Focal neurological deficits

    Science.gov (United States)

    ... or head Electromyogram (EMG), nerve conduction velocities (NCV) MRI of the back, neck, or head Spinal tap Alternative Names Neurological deficits - focal Images Brain References Daroff RB, Jankovic ...

  1. The gyri of the octopus vertical lobe have distinct neurochemical identities.

    Science.gov (United States)

    Shigeno, Shuichi; Ragsdale, Clifton W

    2015-06-15

    The cephalopod vertical lobe is the largest learning and memory structure known in invertebrate nervous systems. It is part of the visual learning circuit of the central brain, which also includes the superior frontal and subvertical lobes. Despite the well-established functional importance of this system, little is known about neuropil organization of these structures and there is to date no evidence that the five longitudinal gyri of the vertical lobe, perhaps the most distinctive morphological feature of the octopus brain, differ in their connections or molecular identities. We studied the histochemical organization of these structures in hatchling and adult Octopus bimaculoides brains with immunostaining for serotonin, octopus gonadotropin-releasing hormone (oGNRH), and octopressin-neurophysin (OP-NP). Our major finding is that the five lobules forming the vertical lobe gyri have distinct neurochemical signatures. This is most prominent in the hatchling brain, where the median and mediolateral lobules are enriched in OP-NP fibers, the lateral lobule is marked by oGNRH innervation, and serotonin immunostaining heavily labels the median and lateral lobules. A major source of input to the vertical lobe is the superior frontal lobe, which is dominated by a neuropil of interweaving fiber bundles. We have found that this neuropil also has an intrinsic neurochemical organization: it is partitioned into territories alternately enriched or impoverished in oGNRH-containing fascicles. Our findings establish that the constituent lobes of the octopus superior frontal-vertical system have an intricate internal anatomy, one likely to reflect the presence of functional subsystems within cephalopod learning circuitry. © 2015 Wiley Periodicals, Inc.

  2. Neurochemical changes in the hippocampus and prefrontal cortex associated with electroacupuncture for learning and memory impairment.

    Science.gov (United States)

    He, Jian; Zhao, Congkuai; Liu, Weilin; Huang, Jia; Liang, Shengxiang; Chen, Lidian; Tao, Jing

    2018-02-01

    Electroacupuncture (EA) has been widely used to treat cognitive impairment following cerebral ischemia. However, the functional mechanisms of EA have not been fully elucidated. The aim of the present study was to investigate whether EA at the GV 20 and DU 24 acupoints can improve the learning and memory ability via alteration of the neurochemical metabolism in the hippocampus (HPC) and prefrontal cortex (PFC) of rats with ischemia and reperfusion (I/R) injury. Sprague‑Dawley male rats were randomly divided into three groups, namely the sham group (n=12), the middle cerebral artery occlusion (MCAO) group (n=12) and the EA treatment (MCAO + EA) group (n=12). MCAO was performed to establish the left focal cerebral I/R injury model, and the GV 20 and DU 24 acupoints were then stimulated with EA for 30 min per time, once daily, for 7 consecutive days. The Morris water maze (MWM) test was used to assess learning and memory ability. T2‑weighted imaging was used to assess the cerebral infarct volume. Magnetic resonance spectroscopy was used to assess neurochemical metabolism of HPC and PFC. The neurological scores of the MCAO + EA group were significantly reduced compared with those of the MCAO group 7 days after EA treatment (Pplatform area was significantly higher in the MCAO + EA group compared with that in the MCAO group (P0.05). The ratios of NAA/Cr, Cho/Cr and Glu/Cr of left‑to‑right PFC were elevated (Plearning and memory ability, possibly through increasing the levels of NAA and Cho in the HPC and PFC of rats with I/R injury.

  3. REM sleep deprivation reverses neurochemical and other depressive-like alterations induced by olfactory bulbectomy.

    Science.gov (United States)

    Maturana, Maira J; Pudell, Cláudia; Targa, Adriano D S; Rodrigues, Laís S; Noseda, Ana Carolina D; Fortes, Mariana H; Dos Santos, Patrícia; Da Cunha, Cláudio; Zanata, Sílvio M; Ferraz, Anete C; Lima, Marcelo M S

    2015-02-01

    There is compelling evidence that sleep deprivation (SD) is an effective strategy in promoting antidepressant effects in humans, whereas few studies were performed in relevant animal models of depression. Acute administration of antidepressants in humans and rats generates a quite similar effect, i.e., suppression of rapid eye movement (REM) sleep. Then, we decided to investigate the neurochemical alterations generated by a protocol of rapid eye movement sleep deprivation (REMSD) in the notably known animal model of depression induced by the bilateral olfactory bulbectomy (OBX). REMSD triggered antidepressant mechanisms such as the increment of brain-derived neurotrophic factor (BDNF) levels, within the substantia nigra pars compacta (SNpc), which were strongly correlated to the swimming time (r = 0.83; P < 0.0001) and hippocampal serotonin (5-HT) content (r = 0.66; P = 0.004). Moreover, there was a strong correlation between swimming time and hippocampal 5-HT levels (r = 0.70; P = 0.003), strengthen the notion of an antidepressant effect associated to REMSD in the OBX rats. In addition, REMSD robustly attenuated the hippocampal 5-HT deficiency produced by the OBX procedure. Regarding the rebound (REB) period, we observed the occurrence of a sustained antidepressant effect, indicated mainly by the swimming and climbing times which could be explained by the maintenance of the increased nigral BDNF expression. Hence, hippocampal 5-HT levels remained enhanced in the OBX group after this period. We suggested that the neurochemical complexity inflicted by the OBX model, counteracted by REMSD, is directly correlated to the nigral BDNF expression and hippocampal 5-HT levels. The present findings provide new information regarding the antidepressant mechanisms triggered by REMSD.

  4. Previous Ketamine Produces an Enduring Blockade of Neurochemical and Behavioral Effects of Uncontrollable Stress

    Science.gov (United States)

    Dolzani, Samuel D.; Tilden, Scott; Christianson, John P.; Kubala, Kenneth H.; Bartholomay, Kristi; Sperr, Katherine; Ciancio, Nicholas; Watkins, Linda R.; Maier, Steven F.

    2016-01-01

    Recent interest in the antidepressant and anti-stress effects of subanesthetic doses of ketamine, an NMDA receptor antagonist, has identified mechanisms whereby ketamine reverses the effect of stress, but little is known regarding the prophylactic effect ketamine might have on future stressors. Here we investigate the prophylactic effect of ketamine against neurochemical and behavioral changes that follow inescapable, uncontrollable tail shocks (ISs) in Sprague Dawley rats. IS induces increased anxiety, which is dependent on activation of serotonergic (5-HT) dorsal raphe nucleus (DRN) neurons that project to the basolateral amygdala (BLA). Ketamine (10 mg/kg, i.p.) administered 2 h, 1 week, or 2 weeks before IS prevented the increased extracellular levels of 5-HT in the BLA typically produced by IS. In addition, ketamine administered at these time points blocked the decreased juvenile social investigation produced by IS. Microinjection of ketamine into the prelimbic (PL) region of the medial prefrontal cortex duplicated the effects of systemic ketamine, and, conversely, systemic ketamine effects were prevented by pharmacological inhibition of the PL. Although IS does not activate DRN-projecting neurons from the PL, IS did so after ketamine, suggesting that the prophylactic effect of ketamine is a result of altered functioning of this projection. SIGNIFICANCE STATEMENT The reported data show that systemic ketamine, given up to 2 weeks before a stressor, blunts behavioral and neurochemical effects of the stressor. The study also advances understanding of the mechanisms involved and suggests that ketamine acts at the prelimbic cortex to sensitize neurons that project to and inhibit the DRN. PMID:26740657

  5. Rapid sensing of l-leucine by human and murine hypothalamic neurons: Neurochemical and mechanistic insights.

    Science.gov (United States)

    Heeley, Nicholas; Kirwan, Peter; Darwish, Tamana; Arnaud, Marion; Evans, Mark L; Merkle, Florian T; Reimann, Frank; Gribble, Fiona M; Blouet, Clemence

    2018-02-07

    Dietary proteins are sensed by hypothalamic neurons and strongly influence multiple aspects of metabolic health, including appetite, weight gain, and adiposity. However, little is known about the mechanisms by which hypothalamic neural circuits controlling behavior and metabolism sense protein availability. The aim of this study is to characterize how neurons from the mediobasal hypothalamus respond to a signal of protein availability: the amino acid l-leucine. We used primary cultures of post-weaning murine mediobasal hypothalamic neurons, hypothalamic neurons derived from human induced pluripotent stem cells, and calcium imaging to characterize rapid neuronal responses to physiological changes in extracellular l-Leucine concentration. A neurochemically diverse subset of both mouse and human hypothalamic neurons responded rapidly to l-leucine. Consistent with l-leucine's anorexigenic role, we found that 25% of mouse MBH POMC neurons were activated by l-leucine. 10% of MBH NPY neurons were inhibited by l-leucine, and leucine rapidly reduced AGRP secretion, providing a mechanism for the rapid leucine-induced inhibition of foraging behavior in rodents. Surprisingly, none of the candidate mechanisms previously implicated in hypothalamic leucine sensing (K ATP channels, mTORC1 signaling, amino-acid decarboxylation) were involved in the acute activity changes produced by l-leucine. Instead, our data indicate that leucine-induced neuronal activation involves a plasma membrane Ca 2+ channel, whereas leucine-induced neuronal inhibition is mediated by inhibition of a store-operated Ca 2+ current. A subset of neurons in the mediobasal hypothalamus rapidly respond to physiological changes in extracellular leucine concentration. Leucine can produce both increases and decreases in neuronal Ca 2+ concentrations in a neurochemically-diverse group of neurons, including some POMC and NPY/AGRP neurons. Our data reveal that leucine can signal through novel mechanisms to rapidly

  6. Sensory receptors in the visceral pleura: neurochemical coding and live staining in whole mounts.

    Science.gov (United States)

    Pintelon, Isabel; Brouns, Inge; De Proost, Ian; Van Meir, Frans; Timmermans, Jean-Pierre; Adriaensen, Dirk

    2007-05-01

    Today, diagnosis and treatment of chest pain related to pathologic changes in the visceral pleura are often difficult. Data in the literature on the sensory innervation of the visceral pleura are sparse. The present study aimed at identifying sensory end-organs in the visceral pleura, and at obtaining more information about neurochemical coding. The immunocytochemcial data are mainly based on whole mounts of the visceral pleura of control and vagally denervated rats. It was shown that innervation of the rat visceral pleura is characterized by nerve bundles that enter in the hilus region and gradually split into slender bundles with a few nerve fibers. Separate nerve fibers regularly give rise to characteristic laminar terminals. Because of their unique association with the elastic fibers of the visceral pleura, we decided to refer to them as "visceral pleura receptors" (VPRs). Cryostat sections of rat lungs confirmed a predominant location on mediastinal and interlobar lung surfaces. VPRs can specifically be visualized by protein gene product 9.5 immunostaining, and were shown to express vesicular glutamate transporters, calbindin D28K, Na+/K+-ATPase, and P2X3 ATP-receptors. The sensory nerve fibers giving rise to VPRs appeared to be myelinated and to have a spinal origin. Because several of the investigated proteins have been reported as markers for sensory terminals in other organs, the present study revealed that VPRs display the neurochemical characteristics of mechanosensory and/or nociceptive terminals. The development of a live staining method, using AM1-43, showed that VPRs can be visualized in living tissue, offering an interesting model for future physiologic studies.

  7. Mercury exposure and neurochemical biomarkers in multiple brain regions of Wisconsin river otters (Lontra canadensis).

    Science.gov (United States)

    Dornbos, Peter; Strom, Sean; Basu, Niladri

    2013-04-01

    River otters are fish-eating wildlife that bioaccumulate high levels of mercury (Hg). Mercury is a proven neurotoxicant to mammalian wildlife, but little is known about the underlying, sub-clinical effects. Here, the overall goal was to increase understanding of Hg's neurological risk to otters. First, Hg values across several brain regions and tissues were characterized. Second, in three brain regions with known sensitivity to Hg (brainstem, cerebellum, and occipital cortex), potential associations among Hg levels and neurochemical biomarkers [N-methyl-D-aspartic acid (NMDA) and gamma-aminobutyric acid (GABAA) receptor] were explored. There were no significant differences in Hg levels across eight brain regions (rank order, highest to lowest: frontal cortex, cerebellum, temporal cortex, occipital cortex, parietal cortex, basal ganglia, brainstem, and thalamus), with mean values ranging from 0.7 to 1.3 ug/g dry weight. These brain levels were significantly lower than mean values in the muscle (2.1 ± 1.4 ug/g), liver (4.7 ± 4.3 ug/g), and fur (8.8 ± 4.8 ug/g). While a significant association was found between Hg and NMDA receptor levels in the brain stem (P = 0.028, rp = -0.293), no relationships were found in the cerebellum and occipital cortex. For the GABA receptor, no relationships were found. The lack of consistent Hg-associated neurochemical changes is likely due to low brain Hg levels in these river otters, which are amongst the lowest reported.

  8. Age-related neurochemical changes in the rhesus macaque cochlear nucleus.

    Science.gov (United States)

    Gray, Daniel T; Engle, James R; Recanzone, Gregg H

    2014-05-01

    Neurochemical changes in the expression of various proteins within the central auditory system have been associated with natural aging. These changes may compensate in part for the loss of auditory sensitivity arising from two phenomena of the aging auditory system: cochlear histopathologies and increased excitability of central auditory neurons. Recent studies in the macaque monkey have revealed age-related changes in the density of nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase (NADPHd) and parvalbumin (PV)-positive cells within the inferior colliculus and superior olivary complex. The cochlear nucleus (CN), which is the first central auditory nucleus, remains unstudied. Since the CN participates in the generation of the auditory brainstem response (ABR) and receives direct innervation from the cochlea, it serves as an ideal nucleus to compare the relationship between these neurochemical changes and the physiological and peripheral changes of the aging auditory system. We used stereological sampling to calculate the densities of NADPHd and PV reactive neurons within the three subdivisions of the CN in middle-aged and aged rhesus macaques. Regression analyses of these values with ABR properties and cochlear histopathologies revealed relationships between these cell types and the changing characteristics of the aging auditory system. Our results indicate that NADPHd expression does change with age in a specific subdivision of the CN, but PV does not. Conversely, PV expression correlated with ABR amplitudes and outer hair cell loss in the cochlea, but NADPHd did not. These results indicate that NADPHd and PV may take part in distinct compensatory efforts of the aging auditory system. Copyright © 2013 Wiley Periodicals, Inc.

  9. The trace amine-associated receptor 1 modulates methamphetamine’s neurochemical and behavioural effects

    Directory of Open Access Journals (Sweden)

    Rachel eCotter

    2015-02-01

    Full Text Available The newly discovered trace amine-associated receptor 1 (TAAR1 has the ability to regulate both dopamine function and psychostimulant action. Here, we tested in rats the ability of RO5203648, a selective TAAR1 partial agonist, to modulate the physiological and behavioural effects of methamphetamine (METH. In experiment 1, RO5203468 dose- and time-dependently altered METH-induced locomotor activity, manifested as an early attenuation followed by a late potentiation of METH’s stimulating effects. In experiment 2, rats received a 14-day treatment regimen during which RO5203648 was co-administered with METH. RO5203648 dose-dependently attenuated METH-stimulated hyperactivity, with the effects becoming more apparent as the treatments progressed. After chronic exposure and 3-day withdrawal, rats were tested for locomotor sensitization. RO5203648 administration during the sensitizing phase prevented the development of METH sensitization. However, RO5203648, at the high dose, cross-sensitized with METH. In experiment 3, RO5203648 dose-dependently blocked METH self-administration without affecting operant responding maintained by sucrose, and exhibited lack of reinforcing efficacy when tested as a METH’s substitute. Neurochemical data showed that RO5203648 did not affect METH-mediated DA efflux and uptake inhibition in striatal synaptosomes. In vivo, however, RO5203648 was able to transiently inhibit METH-induced accumulation of extracellular DA levels in the nucleus accumbens. Taken together, these data highlight the significant potential of TAAR1 to modulate METH’s neurochemical and behavioural effects.

  10. Reverse translation of the rodent 5C-CPT reveals that the impaired attention of people with schizophrenia is similar to scopolamine-induced deficits in mice.

    Science.gov (United States)

    Young, J W; Geyer, M A; Rissling, A J; Sharp, R F; Eyler, L T; Asgaard, G L; Light, G A

    2013-11-12

    Attentional dysfunction in schizophrenia (SZ) is a core deficit that contributes to multiple cognitive deficits and the resulting functional disability. However, developing procognitive therapeutics for neuropsychiatric disorders have been limited by a 'translational gap'--a lack of cognitive paradigms having cross-species translational validity and relevance. The present study was designed to perform an initial validation of the cross-species homology of the 5-choice Continuous Performance Test (5C-CPT) in healthy nonpsychiatric comparison subjects (NCS), SZ patients and mice under pharmacologic challenge. The 5C-CPT performance in SZ patients (n=20) was compared with age-matched NCS (n=23). The effects of the general muscarinic receptor antagonist scopolamine on mice (n=21) performing the 5C-CPT were also assessed. SZ subjects exhibited significantly impaired attention in the 5C-CPT, driven by reduced target detection over time and nonsignificantly increased impulsive responding. Similarly, scopolamine significantly impaired attention in mice, driven by reduced target detection and nonsignificantly increased impulsive responding. Scopolamine also negatively affected accuracy and speed of responding in mice, although these measures failed to differentiate SZ vs. NCS. Thus, mice treated with scopolamine exhibited similar impairments in vigilance as seen in SZ, although the differences between the behavioral profiles warrant further study. The availability of rodent and human versions of this paradigm provides an opportunity to: (1) investigate the neuroanatomic, neurochemical and genomic architecture of abnormalities in attention observed in clinical populations such as SZ; (2) develop and refine animal models of cognitive impairments; and (3) improve cross-species translational testing for the development of treatments for these impairments.

  11. Influences of Chronic Mild Stress Exposure on Motor, Non-Motor Impairments and Neurochemical Variables in Specific Brain Areas of MPTP/Probenecid Induced Neurotoxicity in Mice.

    Science.gov (United States)

    Janakiraman, Udaiyappan; Manivasagam, Thamilarasan; Thenmozhi, Arokiasamy Justin; Essa, Musthafa Mohamed; Barathidasan, Rajamani; SaravanaBabu, Chidambaram; Guillemin, Gilles J; Khan, Mohammed A S

    2016-01-01

    Parkinson's disease (PD) is regarded as a movement disorder mainly affecting the elderly population and occurs due to progressive loss of dopaminergic (DAergic) neurons in nigrostriatal pathway. Patients suffer from non-motor symptoms (NMS) such as depression, anxiety, fatigue and sleep disorders, which are not well focussed in PD research. Depression in PD is a predominant /complex symptom and its pathology lies exterior to the nigrostriatal system. The main aim of this study is to explore the causative or progressive effect of chronic mild stress (CMS), a paradigm developed as an animal model of depression in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (25 mg/kg. body wt.) with probenecid (250 mg/kg, s.c.) (MPTP/p) induced mice model of PD. After ten i.p. injections (once in 3.5 days for 5 weeks) of MPTP/p or exposure to CMS for 4 weeks, the behavioural (motor and non-motor) impairments, levels and expressions of dopamine (DA), serotonin (5-HT), DAergic markers such as tyrosine hydroxylase (TH), dopamine transporter (DAT), vesicular monoamine transporters-2 (VMAT 2) and α-synuclein in nigrostriatal (striatum (ST) and substantia nigra (SN)) and extra-nigrostriatal (hippocampus, cortex and cerebellum) tissues were analysed. Significantly decreased DA and 5-HT levels, TH, DAT and VMAT 2 expressions and increased motor deficits, anhedonia-like behaviour and α-synuclein expression were found in MPTP/p treated mice. Pre and/or post exposure of CMS to MPTP/p mice further enhanced the MPTP/p induced DA and 5-HT depletion, behaviour abnormalities and protein expressions. Our results could strongly confirm that the exposure of stress after MPTP/p injections worsens the symptoms and neurochemicals status of PD.

  12. Influences of Chronic Mild Stress Exposure on Motor, Non-Motor Impairments and Neurochemical Variables in Specific Brain Areas of MPTP/Probenecid Induced Neurotoxicity in Mice.

    Directory of Open Access Journals (Sweden)

    Udaiyappan Janakiraman

    Full Text Available Parkinson's disease (PD is regarded as a movement disorder mainly affecting the elderly population and occurs due to progressive loss of dopaminergic (DAergic neurons in nigrostriatal pathway. Patients suffer from non-motor symptoms (NMS such as depression, anxiety, fatigue and sleep disorders, which are not well focussed in PD research. Depression in PD is a predominant /complex symptom and its pathology lies exterior to the nigrostriatal system. The main aim of this study is to explore the causative or progressive effect of chronic mild stress (CMS, a paradigm developed as an animal model of depression in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (25 mg/kg. body wt. with probenecid (250 mg/kg, s.c. (MPTP/p induced mice model of PD. After ten i.p. injections (once in 3.5 days for 5 weeks of MPTP/p or exposure to CMS for 4 weeks, the behavioural (motor and non-motor impairments, levels and expressions of dopamine (DA, serotonin (5-HT, DAergic markers such as tyrosine hydroxylase (TH, dopamine transporter (DAT, vesicular monoamine transporters-2 (VMAT 2 and α-synuclein in nigrostriatal (striatum (ST and substantia nigra (SN and extra-nigrostriatal (hippocampus, cortex and cerebellum tissues were analysed. Significantly decreased DA and 5-HT levels, TH, DAT and VMAT 2 expressions and increased motor deficits, anhedonia-like behaviour and α-synuclein expression were found in MPTP/p treated mice. Pre and/or post exposure of CMS to MPTP/p mice further enhanced the MPTP/p induced DA and 5-HT depletion, behaviour abnormalities and protein expressions. Our results could strongly confirm that the exposure of stress after MPTP/p injections worsens the symptoms and neurochemicals status of PD.

  13. Neurochemical features of endomorphin-2-containing neurons in the submucosal plexus of the rat colon.

    Science.gov (United States)

    Li, Jun-Ping; Zhang, Ting; Gao, Chang-Jun; Kou, Zhen-Zhen; Jiao, Xu-Wen; Zhang, Lian-Xiang; Wu, Zhen-Yu; He, Zhong-Yi; Li, Yun-Qing

    2015-09-14

    To investigate the distribution and neurochemical phenotype of endomorphin-2 (EM-2)-containing neurons in the submucosal plexus of the rat colon. The mid-colons between the right and left flexures were removed from rats, and transferred into Kreb's solution. For whole-mount preparations, the mucosal, outer longitudinal muscle and inner circular muscle layers of the tissues were separated from the submucosal layer attached to the submucosal plexus. The whole-mount preparations from each rat mid-colon were mounted onto seven gelatin-coated glass slides, and processed for immunofluorescence histochemical double-staining of EM-2 with calcitonin gene-related peptide (CGRP), choline acetyltransferase (ChAT), nitric oxide synthetase (NOS), neuron-specific enolase (NSE), substance P (SP) and vasoactive intestinal peptide (VIP). After staining, all the fluorescence-labeled sections were observed with a confocal laser scanning microscope. To estimate the extent of the co-localization of EM-2 with CGRP, ChAT, NOS, NSE, SP and VIP, ganglia, which have a clear boundary and neuronal cell outline, were randomly selected from each specimen for this analysis. In the submucosal plexus of the mid-colon, many EM-2-immunoreactive (IR) and NSE-IR neuronal cell bodies were found in the submucosal plexus of the rat mid-colon. Approximately 6 ± 4.2 EM-2-IR neurons aggregated within each ganglion and a few EM-2-IR neurons were also found outside the ganglia. The EM-2-IR neurons were also immunopositive for ChAT, SP, VIP or NOS. EM-2-IR nerve fibers coursed near ChAT-IR neurons, and some of these fibers were even distributed around ChAT-IR neuronal cell bodies. Some EM-2-IR neuronal cell bodies were surrounded by SP-IR nerve fibers, but many long processes connecting adjacent ganglia were negative for EM-2 immunostaining. Long VIP-IR processes with many branches coursed through the ganglia and surrounded the EM-2-IR neurons. The percentages of the EM-2-IR neurons that were also positive for

  14. Women and Budget Deficits

    OpenAIRE

    Signe Krogstrup; Sébastien Wälti

    2007-01-01

    If women have different economic preferences than men, then female economic and political empowerment is likely to change policy and household decisions, and in turn macroeconomic outcomes. We test the hypothesis that female enfranchisement leads to lower government budget deficits due gender differences in preferences over fiscal outcomes. Estimating the impact of women's vote on budget deficits in a differences-in-differences regression for Swiss cantonal panel data, we find that including ...

  15. From genes to behavior: investigations of neurochemical signaling come of age for the model crustacean Daphnia pulex.

    Science.gov (United States)

    Christie, Andrew E; McCoole, Matthew D

    2012-08-01

    The cladoceran crustacean Daphnia pulex has served as a standard organism for aquatic toxicity testing for decades. The model organism status of D. pulex rests largely on its remarkable ability to rapidly adapt morphologically, physiologically and behaviorally to a wide range of environmental challenges, as well as on its parthenogenetic reproduction and ease of laboratory culture. As in all multicellular organisms, neurochemical control systems are undoubtedly major contributors to the functional flexibility of Daphnia. Surprisingly, little work has focused on understanding its neurochemistry at any level. Recently, D. pulex has been the subject of extensive genome and transcriptome sequencing, and it is currently the only crustacean with a fully sequenced, publicly accessible genome. Although the molecular work was initiated for gene-based investigations of ecotoxicology and toxicogenomics, the data generated have allowed for investigations into numerous aspects of Daphnia biology, including its neurochemical signaling. This Commentary summarizes our knowledge of D. pulex neurochemistry obtained from recent genomic and transcriptomic studies, and places these data in context with other anatomical, biochemical and physiological experiments using D. pulex and its sister species Daphnia magna. Suggestions as to how the Daphnia molecular data may be useful for future investigations of crustacean neurochemical signaling are also provided.

  16. Effects of melatonin on aluminium-induced neurobehavioral and neurochemical changes in aging rats.

    Science.gov (United States)

    Allagui, M S; Feriani, A; Saoudi, M; Badraoui, R; Bouoni, Z; Nciri, R; Murat, J C; Elfeki, A

    2014-08-01

    This study aimed to investigate the potential protective effects of melatonin (Mel) against aluminium-induced neurodegenerative changes in aging Wistar rats (24-28months old). Herein, aluminium chloride (AlCl3) (50mg/kg BW/day) was administered by gavage, and melatonin (Mel) was co-administered to a group of Al-treated rats by an intra-peritoneal injection at a daily dose of 10mg/kg BW for four months. The findings revealed that aluminium administration induced a significant decrease in body weight associated with marked mortality for the old group of rats, which was more pronounced in old Al-treated rats. Behavioural alterations were assessed by 'open fields', 'elevated plus maze' and 'Radial 8-arms maze' tests. The results demonstrated that Mel co-administration alleviated neurobehavioral changes in both old and old Al-treated rats. Melatonin was noted to play a good neuroprotective role, reducing lipid peroxidation (TBARs), and enhancing enzymatic (SOD, CAT and GPx) activities in the brain organs of old control and old Al-treated rats. Mel treatment also reversed the decrease of AChE activity in the brain tissues, which was confirmed by histological sections. Overall, the results showed that Mel administration can induce beneficial effects for the treatment of Al-induced neurobehavioral and neurochemical changes in the central nervous system (CNS). Copyright © 2014 Elsevier Ltd. All rights reserved.

  17. Genetic or pharmacological blockade of noradrenaline synthesis enhances the neurochemical, behavioural, and neurotoxic effects of methamphetamine

    Science.gov (United States)

    Weinshenker, David; Ferrucci, Michela; Busceti, Carla L.; Biagioni, Francesca; Lazzeri, Gloria; Liles, L. Cameron; Lenzi, Paola; Murri, Luigi; Paparelli, Antonio; Fornai, Francesco

    2008-01-01

    N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) lesions of the locus coeruleus (LC), the major brain noradrenergic nucleus, exacerbate the damage to nigrostriatal dopamine (DA) terminals caused by the psychostimulant methamphetamine (METH). However, because noradrenergic terminals contain other neuromodulators and the noradrenaline (NA) transporter, which may act as a neuroprotective buffer, it was unclear whether this enhancement of METH neurotoxicity was caused by the loss of noradrenergic innervation or the loss of NA itself. We addressed the specific role of NA by comparing the effects of METH in mice with noradrenergic lesions (DSP-4) and those with intact noradrenergic terminals but specifically lacking NA (genetic or acute pharmacological blockade of the NA biosynthetic enzyme dopamine β-hydroxylase; DBH). We found that genetic deletion of DBH (DBH −/− mice) and acute treatment of wild-type mice with a DBH inhibitor (fusaric acid) recapitulated the effects of DSP-4 lesions on METH responses. All three methods of NA depletion enhanced striatal DA release, extracellular oxidative stress (as measured by in vivo microdialysis of DA and 2,3-dihydroxybenzoic acid), and behavioural stereotypies following repeated METH administration. These effects accompanied a worsening of the striatal DA neuron terminal damage and ultrastructural changes to medium spiny neurons. We conclude that NA itself is neuroprotective and plays a fundamental role in the sensitivity of striatal DA terminals to the neurochemical, behavioural, and neurotoxic effects of METH. PMID:18042179

  18. Genetic or pharmacological blockade of noradrenaline synthesis enhances the neurochemical, behavioral, and neurotoxic effects of methamphetamine.

    Science.gov (United States)

    Weinshenker, David; Ferrucci, Michela; Busceti, Carla L; Biagioni, Francesca; Lazzeri, Gloria; Liles, L Cameron; Lenzi, Paola; Pasquali, Livia; Murri, Luigi; Paparelli, Antonio; Fornai, Francesco

    2008-04-01

    N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) lesions of the locus coeruleus, the major brain noradrenergic nucleus, exacerbate the damage to nigrostriatal dopamine (DA) terminals caused by the psychostimulant methamphetamine (METH). However, because noradrenergic terminals contain other neuromodulators and the noradrenaline (NA) transporter, which may act as a neuroprotective buffer, it was unclear whether this enhancement of METH neurotoxicity was caused by the loss of noradrenergic innervation or the loss of NA itself. We addressed the specific role of NA by comparing the effects of METH in mice with noradrenergic lesions (DSP-4) and those with intact noradrenergic terminals but specifically lacking NA (genetic or acute pharmacological blockade of the NA biosynthetic enzyme dopamine beta-hydroxylase; DBH). We found that genetic deletion of DBH (DBH-/- mice) and acute treatment of wild-type mice with a DBH inhibitor (fusaric acid) recapitulated the effects of DSP-4 lesions on METH responses. All three methods of NA depletion enhanced striatal DA release, extracellular oxidative stress (as measured by in vivo microdialysis of DA and 2,3-dihydroxybenzoic acid), and behavioral stereotypies following repeated METH administration. These effects accompanied a worsening of the striatal DA neuron terminal damage and ultrastructural changes to medium spiny neurons. We conclude that NA itself is neuroprotective and plays a fundamental role in the sensitivity of striatal DA terminals to the neurochemical, behavioral, and neurotoxic effects of METH.

  19. ETIOLOGY, TRIGGERS AND NEUROCHEMICAL CIRCUITS ASSOCIATED WITH UNEXPECTED, EXPECTED, AND LABORATORY-INDUCED PANIC ATTACKS

    Science.gov (United States)

    Johnson, Philip L.; Federici, Lauren M.; Shekhar, Anantha

    2014-01-01

    Panic disorder (PD) is a severe anxiety disorder that is characterized by recurrent panic attacks (PA), which can be unexpected (uPA, i.e., no clear identifiable trigger) or expected (ePA). Panic typically involves an abrupt feeling of catastrophic fear or distress accompanied by physiological symptoms such as palpitations, racing heart, thermal sensations, and sweating. Recurrent uPA and ePA can also lead to agoraphobia, where subjects with PD avoid situations that were associated with PA. Here we will review recent developments in our understanding of PD, which includes discussions on: symptoms and signs associated with uPA and ePAs; Diagnosis of PD and the new DSM-V; biological etiology such as heritability and gene x environment and gene x hormonal development interactions; comparisons between laboratory and naturally occurring uPAs and ePAs; neurochemical systems that are associated with clinical PAs (e.g. gene associations; targets for triggering or treating PAs), adaptive fear and panic response concepts in the context of new NIH RDoc approach; and finally strengths and weaknesses of translational animal models of adaptive and pathological panic states. PMID:25130976

  20. Tris(2-chloroethyl)phosphate increases ambulatory activity in mice: pharmacological analyses of its neurochemical mechanism.

    Science.gov (United States)

    Umezu, T; Yonemoto, J; Soma, Y; Suzuki, T

    1998-01-01

    The present study was conducted to clarify the acute effect of tris(2-chloroethyl)phosphate (TRCP), an organophosphate flame-retardant, on spontaneous ambulatory activity (AA) in male ICR mice and to examine the neurochemical mechanism of this effect. Single dose administration of 200 mg/kg i.p. of TRCP increased AA in ICR mice. Neither the nicotinic cholinergic antagonist mecamylamine (MA) nor the muscarinic cholinergic antagonist scopolamine (SCP) affected the AA response to TRCP. On the other hand, the benzodiazepine agonist diazepam (DZ), the GABAA agonist muscimol (MUS) and the GABAB agonist baclofen (BAC) all attenuated the effect of TRCP. DZ and MUS blocked the increase of AA within the first 10 min after administration of TRCP. These drugs did not attenuate the AA-increasing effect of SCP, suggesting that the mechanism of TRCP action is distinct from that of SCP. MUS and BAC did, but DZ did not, inhibit the AA increasing effect of the dopaminergic agonist apomorphine (APO), suggesting that dopamine is involved in the control of AA, and that GABA can affect AA through interaction with dopaminergic neurons. These results suggest that TRCP acts as a GABA antagonist and not as a cholinergic agonist, and that TRCP increases AA in ICR mice through a GABAergic mechanism.

  1. Mercury exposure and neurochemical impacts in bald eagles across several Great Lakes states.

    Science.gov (United States)

    Rutkiewicz, Jennifer; Nam, Dong-Ha; Cooley, Thomas; Neumann, Kay; Padilla, Irene Bueno; Route, William; Strom, Sean; Basu, Niladri

    2011-10-01

    In this study, we assessed mercury (Hg) exposure in several tissues (brain, liver, and breast and primary feathers) in bald eagles (Haliaeetus leucocephalus) collected from across five Great Lakes states (Iowa, Michigan, Minnesota, Ohio, and Wisconsin) between 2002-2010, and assessed relationships between brain Hg and neurochemical receptors (NMDA and GABA(A)) and enzymes (glutamine synthetase (GS) and glutamic acid decarboxylase (GAD)). Brain total Hg (THg) levels (dry weight basis) averaged 2.80 μg/g (range: 0.2-34.01), and levels were highest in Michigan birds. THg levels in liver (r(p) = 0.805) and breast feathers (r(p) = 0.611) significantly correlated with those in brain. Brain Hg was not associated with binding to the GABA(A) receptor. Brain THg and inorganic Hg (IHg) were significantly positively correlated with GS activity (THg r(p) = 0.190; IHg r(p) = 0.188) and negatively correlated with NMDA receptor levels (THg r(p) = -0245; IHg r(p) = -0.282), and IHg was negatively correlated with GAD activity (r(s) = -0.196). We also report upon Hg demethylation and relationships between Hg and Se in brain and liver. These results suggest that bald eagles in the Great Lakes region are exposed to Hg at levels capable of causing subclinical neurological damage, and that when tissue burdens are related to proposed avian thresholds approximately 14-27% of eagles studied here may be at risk.

  2. Neurochemical factors underlying individual differences in locomotor activity and anxiety-like behavioral responses in zebrafish.

    Science.gov (United States)

    Tran, Steven; Nowicki, Magda; Muraleetharan, Arrujyan; Chatterjee, Diptendu; Gerlai, Robert

    2016-02-04

    Variation among individuals may arise for several reasons, and may have diverse underlying mechanisms. Individual differences have been studied in a variety of species, but recently a new model organism has emerged in this field that offers both sophistication in phenotypical characterization and powerful mechanistic analysis. Recently, zebrafish, one of the favorites of geneticists, have been shown to exhibit consistent individual differences in baseline locomotor activity. In the current study, we further explore this finding and examine whether individual differences in locomotor activity correlate with anxiety-like behavioral measures and with levels of dopamine, serotonin and the metabolites of these neurotransmitters. In addition, we examine whether individual differences in locomotor activity are also associated with reactivity to the locomotor stimulant effects of and neurochemical responses to acute ethanol exposure (30min long, 1% v/v ethanol bath application). Principal component analyses revealed a strong association among anxiety-like responses, locomotor activity, serotonin and dopamine levels. Furthermore, ethanol exposure was found to abolish the locomotion-dependent anxiety-like behavioral and serotonergic responses suggesting that this drug also engages a common underlying pathway. Overall, our results provide support for an important role of the serotonergic system in mediating individual differences in anxiety-like responses and locomotor activity in zebrafish and for a minor modulatory role of the dopaminergic system. Copyright © 2015 Elsevier Inc. All rights reserved.

  3. Neurochemical imaging of Alzheimer`s disease and other degenerative dementias

    Energy Technology Data Exchange (ETDEWEB)

    Frey, K.A.; Minoshima, S.; Kuhl, D.E. [Ann Arbor, Univ. of Michigan, MI (United States). Dept. of Internal Medicine. Division of Nuclear Medicine

    1998-09-01

    A wide variety of neurochemical and functional imaging approaches have been applied to the study of progressive dementias, particularly Alzheimer`s disease (Ad) and related disorders. Despite considerable progress in the past decade, the cause(s) of most cases of Ad remain undetermined and preventive or protective therapies are lacking. Specifically-designed imaging procedures have permitted the testing of pathophysiological hypotheses of the etiology and progression of Ad, and have yielded important insights in several areas including the potential roles of cerebral cortical cholinergic lesions, cellular inflammation, and losses of cortical synapses. From the perspective of clinical diagnosis, PET glucose metabolism imaging with use of ({sup 18}F)2-fluorodeoxyglucose (FDG) is the most sensitive and specific imaging modality yet identified. The overall performance of PET FDG is favorable for routine clinical evaluation of suspected Ad, and will likely gain increasing utilization in the near future. Assessments of glucose metabolism and other, specific aspects of neurochemistry in Ad will provide direct measures of therapeutic drug actions and may permit distinction of symptomatic versus disease-modifying therapies as they are developed and introduced in clinical trials.

  4. Neurochemical and neuropharmacological aspects of circadian disruptions: an introduction to asynchronization.

    Science.gov (United States)

    Kohyama, Jun

    2011-06-01

    Circadian disruptions are common in modern society, and there is an urgent need for effective treatment strategies. According to standard diagnostic criteria, most adolescents showing both insomnia and daytime sleepiness are diagnosed as having behavioral-induced sleep efficiency syndrome resulting from insomnia due to inadequate sleep hygiene. However, a simple intervention of adequate sleep hygiene often fails to treat them. As a solution to this clinical problem, the present review first overviews the basic neurochemical and neuropharmachological aspects of sleep and circadian rhythm regulation, then explains several circadian disruptions from similar viewpoints, and finally introduces the clinical notion of asynchronization. Asynchronization is designated to explain the pathophysiology/pathogenesis of exhibition of both insomnia and hypersomnia in adolescents, which comprises disturbances in various aspects of biological rhythms. The major triggers for asynchronization are considered to be a combination of light exposure during the night, which disturbs the biological clock and decreases melatonin secretion, as well as a lack of light exposure in the morning, which prohibits normal synchronization of the biological clock to the 24-hour cycle of the earth and decreases the activity of serotonin. In the chronic phase of asynchronization, involvement of both wake- and sleep-promoting systems is suggested. Both conventional and alternative therapeutic approaches for potential treatment of asynchronization are suggested.

  5. Neurochemical changes in the pericalcarine cortex in congenital blindness attributable to bilateral anophthalmia.

    Science.gov (United States)

    Coullon, Gaelle S L; Emir, Uzay E; Fine, Ione; Watkins, Kate E; Bridge, Holly

    2015-09-01

    Congenital blindness leads to large-scale functional and structural reorganization in the occipital cortex, but relatively little is known about the neurochemical changes underlying this cross-modal plasticity. To investigate the effect of complete and early visual deafferentation on the concentration of metabolites in the pericalcarine cortex, (1)H magnetic resonance spectroscopy was performed in 14 sighted subjects and 5 subjects with bilateral anophthalmia, a condition in which both eyes fail to develop. In the pericalcarine cortex, where primary visual cortex is normally located, the proportion of gray matter was significantly greater, and levels of choline, glutamate, glutamine, myo-inositol, and total creatine were elevated in anophthalmic relative to sighted subjects. Anophthalmia had no effect on the structure or neurochemistry of a sensorimotor cortex control region. More gray matter, combined with high levels of choline and myo-inositol, resembles the profile of the cortex at birth and suggests that the lack of visual input from the eyes might have delayed or arrested the maturation of this cortical region. High levels of choline and glutamate/glutamine are consistent with enhanced excitatory circuits in the anophthalmic occipital cortex, which could reflect a shift toward enhanced plasticity or sensitivity that could in turn mediate or unmask cross-modal responses. Finally, it is possible that the change in function of the occipital cortex results in biochemical profiles that resemble those of auditory, language, or somatosensory cortex. Copyright © 2015 the American Physiological Society.

  6. Behavioural and neurochemical assessment of salvinorin A abuse potential in the rat.

    Science.gov (United States)

    Serra, Veronica; Fattore, Liana; Scherma, Maria; Collu, Roberto; Spano, Maria Sabrina; Fratta, Walter; Fadda, Paola

    2015-01-01

    Salvinorin A is a recreational drug derived from Salvia divinorum, a sage species long used as an entheogen. While salvinorin A has potent hallucinogenic properties, its abuse potential has not been assessed consistently in controlled behavioural and neurochemical studies in rodents. This study aimed to assess salvinorin A abuse potential by measuring its capacity to establish and maintain self-administration behaviour and to modify dopamine (DA) levels in the nucleus accumbens (NAcc) of rats. Male Lister Hooded (LH) and Sprague-Dawley (SD) rats were allowed to self-administer salvinorin A (0.5 or 1.0 μg/kg/infusion) intravenously 2 h/day for 20 days under a continuous schedule of reinforcement and lever pressing as operandum. LH rats discriminated between the active and inactive levers but did not reach the acquisition criterion for stable self-administration (≥12 active responses vs ≤5 inactive responses for at least 5 consecutive days). SD rats discriminated between the two levers at the lower dose only but, like LH rats, never acquired stable self-administration behaviour. Systemic salvinorin A increased extracellular DA in the NAcc shell of both LH (at ≥40 μg/kg) and SD rats (at ≥5 μg/kg), but injection into the ventral tegmental area (VTA) induced no significant change in NAcc DA concentration in LH rats and only brief elevations in SD rats. Salvinorin A differs from other commonly abused compounds since although it affects accumbal dopamine transmission, yet it is unable, at least at the tested doses, to sustain stable intravenous self-administration behaviour.

  7. Morphological and neurochemical differences in peptidergic nerve fibers of the mouse vagina.

    Science.gov (United States)

    Barry, Christine M; Ji, Esther; Sharma, Harman; Beukes, Lara; Vilimas, Patricia I; DeGraaf, Yvette C; Matusica, Dusan; Haberberger, Rainer V

    2017-07-01

    The vagina is innervated by a complex arrangement of sensory, sympathetic, and parasympathetic nerve fibers that contain classical transmitters plus an array of neuropeptides and enzymes known to regulate diverse processes including blood flow and nociception. The neurochemical characteristics and distributions of peptide-containing nerves in the mouse vagina are unknown. This study used multiple labeling immunohistochemistry, confocal maging and analysis to investigate the presence and colocalization of the peptides vasoactive intestinal polypeptide (VIP), calcitonin-gene related peptide (CGRP), substance P (SP), neuropeptide tyrosine (NPY), and the nitric oxide synthesizing enzyme neuronal nitric oxide synthase (nNOS) in nerve fibers of the murine vaginal wall. We compared cervical and vulvar areas of the vagina in young nullipara and older multipara C57Bl/6 mice, and identified differences including that small ganglia were restricted to cervical segments, epithelial fibers were mainly present in vulvar segments and most nerve fibers were found in the lamina propria of the cervical region of the vagina, where a higher number of fibers containing immunoreactivity for VIP, CGRP, SP, or nNOS were found. Two populations of VIP-containing fibers were identified: fibers containing CGRP and fibers containing VIP but not CGRP. Differences between young and older mice were present in multiple layers of the vaginal wall, with older mice showing overall loss of innervation of epithelium of the proximal vagina and reduced proportions of VIP, CGRP, and SP containing nerve fibers in the distal epithelium. The distal vagina also showed increased vascularization and perivascular fibers containing NPY. Immunolabeling of ganglia associated with the vagina indicated the likely origin of some peptidergic fibers. Our results reveal regional differences and age- or parity-related changes in innervation of the mouse vagina, effecting the distribution of neuropeptides with diverse roles

  8. Neurochemically defined cell columns in the nucleus prepositus hypoglossi of the cat and monkey.

    Science.gov (United States)

    Baizer, Joan S; Baker, James F

    2006-06-13

    Many studies have shown that the nucleus prepositus hypoglossi (PH) participates with the vestibular nuclear complex, the cerebellum and the oculomotor nuclei in the control of eye movements. We have looked at the neurochemical organization of PH in the cat and monkey using a recently developed antibody, 8B3, that recognizes a chondroitin sulfate proteoglycan. In the cat, immunoreactivity to 8B3 labels a set of cells in PH. On frontal sections, these cells form a cluster that is seen over the entire anterior-posterior (A-P) extent of PH, but the number of cells in the cluster changes with A-P level. Earlier studies have identified an A-P cell column in PH of the cat whose neurons synthesize nitric oxide. We have used both single- and double-label protocols to investigate the relation between the two cell groups. Single-label studies show spatial overlap but that the cells immunoreactive to nitric oxide synthase (nNOS) are more numerous than cells immunoreactive to 8B3. Double-label studies show that all cells immunoreactive to 8B3 were also immunoreactive to nNOS, but, as suggested by the single-label data, there are many nNOS-immunoreactive cells not immunoreactive to 8B3. Populations of 8B3 and nNOS-immunoreactive cells are also found in PH of squirrel and macaque monkeys. The results suggest that nNOS-immunoreactive cells in PH may consist of two functionally different populations.

  9. Enrichment of MCI and early Alzheimer's disease treatment trials using neurochemical and imaging candidate biomarkers.

    LENUS (Irish Health Repository)

    Hampel, H

    2012-02-01

    In the earliest clinical stages of Alzheimer\\'s Disease (AD), when symptoms are mild, clinical diagnosis will still be difficult. AD related molecular mechanisms precede symptoms. Biological markers can serve as early diagnostic indicators, as markers of preclinical pathological change, e.g. underlying mechanisms of action (MoA). Hypothesis based candidates are derived from structural and functional neuroimaging as well as from cerebrospinal fluid (CSF) and plasma. Unbiased exploratory approaches e.g. proteome analysis or rater independent fully automated imaging post-processing methods yield novel candidates. Recent progress in the validation of core feasible imaging and neurochemical biomarkers for functions such as early detection, classification, progression and prediction of AD is summarized. Single core feasible biomarkers can already be used to enrich populations at risk for AD and may be further enhanced using distinct combinations. Some biomarkers are currently in the process of implementation as primary or secondary outcome variables into regulatory guideline documents, e.g. regarding phase II in drug development programs as outcome measures in proof of concept or dose finding studies. There are specific biomarkers available depending on the hypothesized mechanism of action of a medicinal product, e.g. impact on the amyloidogenic cascade or on tauhyperphosphorylation. Ongoing large-scale international controlled multi-center trials will provide further validation of selected core feasible imaging and CSF biomarker candidates as outcome measures in early AD for use in phase III clinical efficacy trials. There is a need of rigorous co-development of biological trait- and statemarker candidates facilitated through planned synergistic collaboration between academic, industrial and regulatory partners.

  10. Social vs. environmental stress models of depression from a behavioural and neurochemical approach.

    Science.gov (United States)

    Venzala, E; García-García, A L; Elizalde, N; Tordera, R M

    2013-07-01

    Major depression is a mental disorder often preceded by exposure to chronic stress or stressful life events. Recently, animal models based on social conflict such as chronic social defeat stress (CSDS) are proposed to be more relevant to stress-induced human psychopathology compared to environmental models like the chronic mild stress (CMS). However, while CMS reproduces specifically core depressive symptoms such as anhedonia and helplessness, CSDS studies rely on the analysis of stress-induced social avoidance, addressing different neuropsychiatric disorders. Here, we study comparatively the two models from a behavioural and neurochemical approach and their possible relevance to human depression. Mice (C57BL/6) were exposed to CMS or CSDS for six weeks and ten days. Anhedonia was periodically evaluated. A battery of test applied during the fourth week after the stress procedure included motor activity, memory, anxiety, social interaction and helplessness. Subsequently, we examined glutamate, GABA, 5-HT and dopamine levels in the prefrontal cortex, hippocampus and brainstem. CMS induced a clear depressive-like profile including anhedonia, helplessness and memory impairment. CSDS induced anhedonia, hyperactivity, anxiety and social avoidance, signs also common to anxiety and posttraumatic stress disorders. While both models disrupted the excitatory inhibitory balance in the prefrontal cortex, CMS altered importantly this balance in the brainstem. Moreover, CSDS decreased dopamine in the prefrontal cortex and brainstem. We suggests that while depressive-like behaviours might be associated to altered aminoacid neurotransmission in cortical and brain stem areas, CSDS induced anxiety behaviours might be linked to specific alteration of dopaminergic pathways involved in rewarding processes. Copyright © 2012 Elsevier B.V. and ECNP. All rights reserved.

  11. Multimodal neuroimaging based classification of autism spectrum disorder using anatomical, neurochemical, and white matter correlates.

    Science.gov (United States)

    Libero, Lauren E; DeRamus, Thomas P; Lahti, Adrienne C; Deshpande, Gopikrishna; Kana, Rajesh K

    2015-05-01

    Neuroimaging techniques, such as fMRI, structural MRI, diffusion tensor imaging (DTI), and proton magnetic resonance spectroscopy (1H-MRS) have uncovered evidence for widespread functional and anatomical brain abnormalities in autism spectrum disorder (ASD) suggesting it to be a system-wide neural systems disorder. Nevertheless, most previous studies have focused on examining one index of neuropathology through a single neuroimaging modality, and seldom using multiple modalities to examine the same cohort of individuals. The current study aims to bring together multiple brain imaging modalities (structural MRI, DTI, and 1H-MRS) to investigate the neural architecture in the same set of individuals (19 high-functioning adults with ASD and 18 typically developing (TD) peers). Morphometry analysis revealed increased cortical thickness in ASD participants, relative to typical controls, across the left cingulate, left pars opercularis of the inferior frontal gyrus, left inferior temporal cortex, and right precuneus, and reduced cortical thickness in right cuneus and right precentral gyrus. ASD adults also had reduced fractional anisotropy (FA) and increased radial diffusivity (RD) for two clusters on the forceps minor of the corpus callosum, revealed by DTI analyses. 1H-MRS results showed a reduction in the N-acetylaspartate/Creatine ratio in dorsal anterior cingulate cortex (dACC) in ASD participants. A decision tree classification analysis across the three modalities resulted in classification accuracy of 91.9% with FA, RD, and cortical thickness as key predictors. Examining the same cohort of adults with ASD and their TD peers, this study found alterations in cortical thickness, white matter (WM) connectivity, and neurochemical concentration in ASD. These findings underscore the potential for multimodal imaging to better inform on the neural characteristics most relevant to the disorder. Copyright © 2015 Elsevier Ltd. All rights reserved.

  12. Neurochemical characterization of neurons expressing melanin-concentrating hormone receptor 1 in the mouse hypothalamus1

    Science.gov (United States)

    Chee, Melissa J. S.; Pissios, Pavlos; Maratos-Flier, Eleftheria

    2013-01-01

    Melanin-concentrating hormone (MCH) is a hypothalamic neuropeptide that acts via MCH receptor 1 (MCHR1) in the mouse. It promotes positive energy balance thus mice lacking MCH or MCHR1 are lean, hyperactive, and resistant to diet-induced obesity. Identifying the cellular targets of MCH is an important step to understanding the mechanisms underlying MCH actions. We generated the Mchr1-cre mouse that expressed cre recombinase driven by the MCHR1 promoter and crossed it with a tdTomato reporter mouse. The resulting Mchr1-cre/tdTomato progeny expressed easily detectable tdTomato fluorescence in MCHR1 neurons, which were found throughout the olfactory system, striatum, and hypothalamus. To chemically identify MCH-targeted cell populations that play a role in energy balance, MCHR1 hypothalamic neurons were characterized by colabeling select hypothalamic neuropeptides with tdTomato fluorescence. TdTomato fluorescence colocalized with dynorphin, oxytocin, vasopressin, enkephalin, thyrothropin-releasing hormone, and corticotropin-releasing factor immunoreactive cells in the paraventricular nucleus. In the lateral hypothalamus, neurotensin but neither orexin nor MCH neurons expressed tdTomato. In the arcuate nucleus, both Neuropeptide Y and proopiomelanocortin cells expressed tdTomato. We further demonstrated that some of these arcuate neurons were also targets of leptin action. Interestingly, MCHR1 was expressed in the vast majority of leptin-sensitive proopiomelanocortin neurons, highlighting their importance for the orexigenic actions of MCH. Taken together, this study supports the use of the Mchr1-cre mouse for outlining the neuroanatomical distribution and neurochemical phenotype of MCHR1 neurons. PMID:23605441

  13. Neurochemical characterization of neurons expressing melanin-concentrating hormone receptor 1 in the mouse hypothalamus.

    Science.gov (United States)

    Chee, Melissa J S; Pissios, Pavlos; Maratos-Flier, Eleftheria

    2013-07-01

    Melanin-concentrating hormone (MCH) is a hypothalamic neuropeptide that acts via MCH receptor 1 (MCHR1) in the mouse. It promotes positive energy balance; thus, mice lacking MCH or MCHR1 are lean, hyperactive, and resistant to diet-induced obesity. Identifying the cellular targets of MCH is an important step to understanding the mechanisms underlying MCH actions. We generated the Mchr1-cre mouse that expresses cre recombinase driven by the MCHR1 promoter and crossed it with a tdTomato reporter mouse. The resulting Mchr1-cre/tdTomato progeny expressed easily detectable tdTomato fluorescence in MCHR1 neurons, which were found throughout the olfactory system, striatum, and hypothalamus. To chemically identify MCH-targeted cell populations that play a role in energy balance, MCHR1 hypothalamic neurons were characterized by colabeling select hypothalamic neuropeptides with tdTomato fluorescence. TdTomato fluorescence colocalized with dynorphin, oxytocin, vasopressin, enkephalin, thyrothropin-releasing hormone, and corticotropin-releasing factor immunoreactive cells in the paraventricular nucleus. In the lateral hypothalamus, neurotensin, but neither orexin nor MCH neurons, expressed tdTomato. In the arcuate nucleus, both Neuropeptide Y and proopiomelanocortin cells expressed tdTomato. We further demonstrated that some of these arcuate neurons were also targets of leptin action. Interestingly, MCHR1 was expressed in the vast majority of leptin-sensitive proopiomelanocortin neurons, highlighting their importance for the orexigenic actions of MCH. Taken together, this study supports the use of the Mchr1-cre mouse for outlining the neuroanatomical distribution and neurochemical phenotype of MCHR1 neurons. Copyright © 2012 Wiley Periodicals, Inc.

  14. Normal neurochemistry in the prefrontal and cerebellar brain of adults with attention-deficit-hyperactivity disorder

    Directory of Open Access Journals (Sweden)

    Dominique eEndres

    2015-09-01

    Full Text Available Attention-deficit-hyperactivity disorder (ADHD is a common neurodevelopmental disorder. In an attempt to extend earlier neurochemical findings, we organized a magnetic resonance spectroscopy (MRS study as part of a large, government-funded, prospective, randomized, multicenter clinical trial comparing the effectiveness of specific psychotherapy with counseling and stimulant treatment with placebo treatment (COMPAS study. We report the baseline neurochemical data for the anterior cingulate cortex (ACC and the cerebellum in a case-control setting. For the trial, 1 480 adult patients were contacted for participation, 518 were assessed for eligibility, 433 were randomized, and 187 were potentially eligible for neuroimaging. The control group included 119 healthy volunteers. Single-voxel proton MRS was performed. In the patient group, 113 ACC and 104 cerebellar spectra fulfilled all quality criteria for inclusion in statistical calculations, as did 82 ACC and 78 cerebellar spectra in the control group. We did not find any significant neurometabolic differences between the ADHD and control group in the ACC (Wilks’ lambda test: p = 0.97 or in the cerebellum (p = 0.62. Thus, we were unable to replicate earlier findings in this methodologically sophisticated study. We discuss our findings in the context of a comprehensive review of other MRS studies on ADHD and a somewhat skeptical neuropsychiatric research perspective. As in other neuropsychiatric disorders, the unclear nosological status of ADHD might be an explanation for false-negative findings.

  15. Cognitive deficits in schizophrenia

    Directory of Open Access Journals (Sweden)

    S Chattopadhyay

    2012-01-01

    Full Text Available The term schizophrenia was coined by Eugene Bleuler. Symptoms of schizophrenia are arranged into groups or clusters called as domains. The domains of dysfunctions are positive symptoms, negative symptoms, cognitive impairments, mood and suicidity, and aggression. Cognition is the sum total of mental processes that makes us acquire knowledge and keeps us aware of our surroundings and thus enables us to arrive at appropriate judgments. Cognitive deficits are recognized as enduring and persistent features in schizophrenia and can be neuro-cognitive or relating to social cognition. Neurocognitive deficits are deficits in speed of processing, attention / vigilance, working memory, verbal memory, visual memory, reasoning and problem solving, social cognition. Cognitive function can be assessed by various methods like experimental approach, neuropsychological and psychometric and ecologic approach. Cognitive deficits are present at onset of illness producing substantial impairment. Unlike psychotic symptoms, which remit with treatment, functional impairments remain stable over time. Detail understanding of such symptoms will help in disability limitation. Various cognitive remediation programmes are underway with such intent. Articles till March, 2012 were searched through PubMed and Google Scholar, which were studied in an attempt of understanding the topic. The information was structured and organized.

  16. Beyond the knowledge deficit

    DEFF Research Database (Denmark)

    Hansen, Janus Staffan; Holm, Lotte; Frewer, Lynn

    2003-01-01

    The paper reviews psychological and social scientific research on lay attitudes to food risks. Many experts (scientists, food producers and public health advisors) regard public unease about food risks as excessive. This expert-lay discrepancy is often attributed to a 'knowledge deficit' among lay...

  17. Ameliorative Effects of Acanthopanax trifoliatus on Cognitive and Emotional Deficits in Olfactory Bulbectomized Mice: An Animal Model of Depression and Cognitive Deficits

    Directory of Open Access Journals (Sweden)

    Pongtip Sithisarn

    2013-01-01

    Full Text Available Acanthopanax trifoliatus is a plant that has been traditionally used in Thailand as a vegetable and a tonic. This study investigated effects of the aqueous extract of its leaves (ATL on cognitive and emotional deficits using an olfactory bulbectomized mouse (OBX model. OBX mice were treated daily with ATL (250 and 500 mg/kg, p.o. 3 days after OBX. Antidementia drug tacrine (2.5 mg/kg/day and antidepressant drug imipramine (10 mg/kg/day were given i.p. as reference drugs. OBX significantly impaired cognitive behavior in a novel object recognition test and a modified Y-maze test and induced depression-like behavior in a tail suspension test. ATL and tacrine treatment attenuated OBX-induced cognitive deficits, whereas ATL and imipramine improved OBX-induced depression-like behavior. Neurochemical studies conducted after completing behavioral experiments demonstrated that OBX downregulated the expression levels of cholinergic marker genes encoding choline acetyltransferase and muscarinic M1 receptor in a manner reversed by ATL and tacrine. Moreover, ATL and tacrine administration inhibited the ex vivo activity of acetylcholinesterase in the brain. These findings suggest that ATL is beneficial for the treatment of cognitive and emotional deficits related to dementia with depressive symptoms and that the antidementia effect of ATL is mediated by normalizing the function of central cholinergic systems.

  18. Effects of serotonin 2C receptor agonists on the behavioral and neurochemical effects of cocaine in squirrel monkeys.

    Science.gov (United States)

    Manvich, Daniel F; Kimmel, Heather L; Howell, Leonard L

    2012-05-01

    Accumulating evidence indicates that the serotonin system modulates the behavioral and neurochemical effects of cocaine, but the receptor subtypes mediating these effects remain unknown. Recent studies have demonstrated that pharmacological activation of the serotonin 2C receptor (5-HT(2C)R) attenuates the behavioral and neurochemical effects of cocaine in rodents, but such compounds have not been systematically evaluated in nonhuman primates. The present experiments sought to determine the impact of pretreatment with the preferential 5-HT(2C)R agonist m-chlorophenylpiperazine (mCPP) and the selective 5-HT(2C)R agonist Ro 60-0175 [(α-S)-6-chloro-5-fluoro-α-methyl-1H-indole-1-ethanamine fumarate] on the behavioral and neurochemical effects of cocaine in squirrel monkeys. In subjects trained to lever-press according to a 300-s fixed-interval schedule of stimulus termination, pretreatment with either 5-HT(2C)R agonist dose-dependently and insurmountably attenuated the behavioral stimulant effects of cocaine. In subjects trained to self-administer cocaine, both compounds dose-dependently and insurmountably attenuated cocaine-induced reinstatement of previously extinguished responding in an antagonist-reversible manner, and the selective agonist Ro 60-0175 also attenuated the reinforcing effects of cocaine during ongoing cocaine self-administration. It is noteworthy that the selective agonist Ro 60-0175 exhibited behavioral specificity because it did not significantly alter nondrug-maintained responding. Finally, in vivo microdialysis studies revealed that pretreatment with Ro 60-0175 caused a reduction of cocaine-induced dopamine increases within the nucleus accumbens, but not the caudate nucleus. These results suggest that 5-HT(2C)R agonists functionally antagonize the behavioral effects of cocaine in nonhuman primates, possibly via a selective modulation of cocaine-induced dopamine increases within the mesolimbic dopamine system and may therefore represent a novel

  19. Expanding neurochemical investigations with multi-modal recording: simultaneous fast-scan cyclic voltammetry, iontophoresis, and patch clamp measurements

    Science.gov (United States)

    Kirkpatrick, D. C.; McKinney, C. J.; Manis, P. B.

    2016-01-01

    Multi-modal recording describes the simultaneous collection of information across distinct domains. Compared to isolated measurements, such studies can more easily determine relationships between varieties of phenomena. This is useful for neurochemical investigations which examine cellular activity in response to changes in the local chemical environment. In this study, we demonstrate a method to perform simultaneous patch clamp measurements with fast-scan cyclic voltammetry (FSCV) using optically isolated instrumentation. A model circuit simulating concurrent measurements was used to predict the electrical interference between instruments. No significant impact was anticipated between methods, and predictions were largely confirmed experimentally. One exception was due to capacitive coupling of the FSCV potential waveform into the patch clamp amplifier. However, capacitive transients measured in whole-cell current clamp recordings were well below the level of biological signals, which allowed the activity of cells to be easily determined. Next, the activity of medium spiny neurons (MSNs) was examined in the presence of an FSCV electrode to determine how the exogenous potential impacted nearby cells. The activities of both resting and active MSNs were unaffected by the FSCV waveform. Additionally, application of an iontophoretic current, used to locally deliver drugs and other neurochemicals, did not affect neighboring cells. Finally, MSN activity was monitored during iontophoretic delivery of glutamate, an excitatory neurotransmitter. Membrane depolarization and cell firing were observed concurrently with chemical changes around the cell resulting from delivery. In all, we show how combined electrophysiological and electrochemical measurements can relate information between domains and increase the power of neurochemical investigations. PMID:27314130

  20. Offsetting deficit conceptualisations: methodological considerations ...

    African Journals Online (AJOL)

    ... nature of student learning experiences in ways that accommodate the influence of various contextual realities brings researchers and their research agendas closer to offsetting deficit conceptualisation. Keywords: deficit discourses, higher education, knowledge recontextualisation, literacy practices, research design.

  1. Attention deficit hyperactivity disorder (ADHD)

    Science.gov (United States)

    ... this page: //medlineplus.gov/ency/article/001551.htm Attention deficit hyperactivity disorder To use the sharing features on this page, please enable JavaScript. Attention deficit hyperactivity disorder (ADHD) is a problem caused by the presence ...

  2. Elevated mercury exposure and neurochemical alterations in little brown bats (Myotis lucifugus) from a site with historical mercury contamination.

    Science.gov (United States)

    Nam, Dong-Ha; Yates, David; Ardapple, Pedro; Evers, David C; Schmerfeld, John; Basu, Niladri

    2012-05-01

    Despite evidence of persistent methylmercury (MeHg) contamination in the South River (Virginia, USA) ecosystem, there is little information concerning MeHg-associated neurological impacts in resident wildlife. Here we determined mercury (Hg) concentrations in tissues of insectivorous little brown bats (Myotis lucifugus) collected from a reference site and a MeHg-contaminated site in the South River ecosystem. We also explored whether neurochemical biomarkers (monoamine oxidase, MAO; acetylcholinesterase, ChE; muscarinic acetylcholine receptor, mAChR; N-methyl-D-aspartate receptor, NMDAR) previously shown to be altered by MeHg in other wildlife were associated with brain Hg levels in these bats. Concentrations of Hg (total and MeHg) in tissues were significantly higher (10-40 fold difference) in South River bats when compared to reference sites. Mean tissue mercury levels (71.9 ppm dw in liver, 7.14 ppm dw in brain, 132 ppm fw in fur) in the South River bats exceed (sub)-clinical thresholds in mammals. When compared to the South River bats, animals from the reference site showed a greater ability to demethylate MeHg in brain (33.1% of total Hg was MeHg vs. 65.5%) and liver (8.9% of total Hg was MeHg vs. 50.8%) thus suggesting differences in their ability to detoxify and eliminate Hg. In terms of Hg-associated neurochemical biomarker responses, interesting biphasic responses were observed with an inflection point between 1 and 5 ppm dw in the brain. In the reference bats Hg-associated decreases in MAO (r = -0.61; p exposures, differences in Hg metabolism, and the importance of the aforementioned neurochemicals in multiple facets of animal health, altered or perhaps even a lack of expected neurochemical responses in Hg-contaminated bats raise questions about the ecological and physiological impacts of Hg on the bat population as well as the broader ecosystem in the South River.

  3. Rapid recovery and altered neurochemical dependence of locomotor central pattern generation following lumbar neonatal spinal cord injury.

    Science.gov (United States)

    Züchner, Mark; Kondratskaya, Elena; Sylte, Camilla B; Glover, Joel C; Boulland, Jean-Luc

    2018-01-15

    Spinal compression injury targeted to the neonatal upper lumbar spinal cord, the region of highest hindlimb locomotor rhythmogenicity, leads to an initial paralysis of the hindlimbs. Behavioural recovery is evident within a few days and approaches normal function within about 3 weeks. Fictive locomotion in the isolated injured spinal cord cannot be elicited by a neurochemical cocktail containing NMDA, dopamine and serotonin 1 day post-injury, but can 3 days post-injury as readily as in the uninjured spinal cord. Low frequency coordinated rhythmic activity can be elicited in the isolated uninjured spinal cord by NMDA + dopamine (without serotonin), but not in the isolated injured spinal cord. In both the injured and uninjured spinal cord, eliciting bona fide fictive locomotion requires the additional presence of serotonin. Following incomplete compression injury in the thoracic spinal cord of neonatal mice 1 day after birth (P1), we previously reported that virtually normal hindlimb locomotor function is recovered within about 3 weeks despite substantial permanent thoracic tissue loss. Here, we asked whether similar recovery occurs following lumbar injury that impacts more directly on the locomotor central pattern generator (CPG). As in thoracic injuries, lumbar injuries caused about 90% neuronal loss at the injury site and increased serotonergic innervation below the injury. Motor recovery was slower after lumbar than thoracic injury, but virtually normal function was attained by P25 in both cases. Locomotor CPG status was tested by eliciting fictive locomotion in isolated spinal cords using a widely used neurochemical cocktail (NMDA, dopamine, serotonin). No fictive locomotion could be elicited 1 day post-injury, but could within 3 days post-injury as readily as in age-matched uninjured control spinal cords. Burst patterning and coordination were largely similar in injured and control spinal cords but there were differences. Notably, in both groups there

  4. Attention deficits and divorce.

    Science.gov (United States)

    Bouchard, Geneviève; Saint-Aubin, Jean

    2014-09-01

    Building on previous work on the role of attention deficits associated with the regulation of executive control in psychiatric disorders, we examine whether these attention deficits are related to an interpersonal disturbance, the experience of divorce. Attentional capacities of 95 randomly selected couples from the general population were measured with a well-established task, the Attentional Network Task, which assesses the efficiency of 3 attention networks (that is, alerting, orienting, and executive control). Among the 190 participants, 32 had experienced a divorce in the past. ANCOVAs were used to compare divorced people in marital or cohabiting unions with people in first unions in their performance on this purely cognitive task. Our findings indicate that divorced people who are currently living in a cohabiting relationship show significantly lower executive control than other adults living as couples, after controlling for sex, age, income, and education. This subgroup of divorced people not only exhibit greater difficulty in responding to some stimuli while ignoring irrelevant ones but also manifest cognitive deficits in conflict resolution. This study highlights the links between attention and the long-term maintenance of intimate relationships. Our results may have important implications for the identification of people at risk for divorce.

  5. Voxel Scale Complex Networks of Functional Connectivity in the Rat Brain: Neurochemical State Dependence of Global and Local Topological Properties

    Directory of Open Access Journals (Sweden)

    Adam J. Schwarz

    2012-01-01

    Full Text Available Network analysis of functional imaging data reveals emergent features of the brain as a function of its topological properties. However, the brain is not a homogeneous network, and the dependence of functional connectivity parameters on neuroanatomical substrate and parcellation scale is a key issue. Moreover, the extent to which these topological properties depend on underlying neurochemical changes remains unclear. In the present study, we investigated both global statistical properties and the local, voxel-scale distribution of connectivity parameters of the rat brain. Different neurotransmitter systems were stimulated by pharmacological challenge (d-amphetamine, fluoxetine, and nicotine to discriminate between stimulus-specific functional connectivity and more general features of the rat brain architecture. Although global connectivity parameters were similar, mapping of local connectivity parameters at high spatial resolution revealed strong neuroanatomical dependence of functional connectivity in the rat brain, with clear differentiation between the neocortex and older brain regions. Localized foci of high functional connectivity independent of drug challenge were found in the sensorimotor cortices, consistent with the high neuronal connectivity in these regions. Conversely, the topological properties and node roles in subcortical regions varied with neurochemical state and were dependent on the specific dynamics of the different functional processes elicited.

  6. Cerebellar neurochemical and histopathological changes in rat model of Parkinson's disease induced by intrastriatal injection of rotenone.

    Science.gov (United States)

    Khadrawy, Yasser A; Mourad, Iman M; Mohammed, Haitham S; Noor, Neveen A; Aboul Ezz, Heba S

    2017-01-01

    The aim of the present work was to investigate the neurochemical changes induced in the cerebellum of rat model of Parkinson's disease (PD). Rats were divided into two groups; control and rat model of PD induced by the intrastriatal injection of rotenone. As compared to control, a significant increase in the excitatory amino acid neurotransmitters; glutamate and aspartate together with a significant decrease in the inhibitory amino acids, GABA, glycine and taurine were observed in the cerebellum of rat model of PD. This was associated with a significant increase in lipid peroxidation, nitric oxide and tumor necrosis factor-α and a significant decrease in reduced glutathione. A significant decrease in acetylcholinesterase and a significant increase in Na+,K+-ATPase were recorded in the cerebellum of rat model of PD. In addition the cerebellar sections from rat model of PD showed marked necrosis of Purkinje cells, irregular damaged cells, cytoplasmic shrinkage, necrosis and perineuronal vacuolation. The present results indicate that the disturbance in the balance between the excitatory and inhibitory amino acids may have a role in the pathogenesis of PD. According to the present neurochemical and histopathological changes, the cerebellum should be taken into consideration during the treatment of PD.

  7. Aging-related rotenone-induced neurochemical and behavioral deficits: role of SIRT2 and redox imbalance, and neuroprotection by AK-7

    Directory of Open Access Journals (Sweden)

    Wang X

    2015-05-01

    Full Text Available Xijin Wang,1 Qiang Guan,2 Meihua Wang,1 Liu Yang,1 Jie Bai,1 Zhiqiang Yan,3 Yuhong Zhang,4 Zhenguo Liu11Department of Neurology, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 2Department of Neurology, Tongji Hospital, Tongji University, 3Shanghai Laboratory Animal Center, Chinese Academy of Sciences, 4Department of Neurology, Shanghai Tenth People’s Hospital, Tongji University, Shanghai, People’s Republic of ChinaAbstract: Aging is one of the strongest risk factors for Parkinson’s disease (PD. SIRT2 has been implicated in the aging process. It is pertinent to investigate the role of SIRT2 in aging-related dopaminergic neurotoxicity and to develop effective therapeutic strategies for PD through the use of aging animals. In this study, we observed that rotenone induced significant behavior abnormality and striatal dopamine depletion in aging rats, while it did not do so in young rats. No significant change in striatal serotonin level was observed in the aging rats after rotenone administration. There was also aging-related rotenone-induced increase in substantia nigra (SN SIRT2 expression in the rats. In addition, there was aging-related rotenone-induced SN malondialdehyde (MDA increase and glutathione (GSH decrease in the rats. No significant changes in cerebellar SIRT2, MDA, or GSH levels were observed in the aging rats after rotenone administration. Striatal dopamine content was significantly inversely correlated with SN SIRT2 expression in the rats. AK-7 significantly diminished striatal dopamine depletion and improved behavior abnormality in the rotenone-treated aging rats. Furthermore, AK-7 significantly decreased MDA content and increased GSH content in the SN of rotenone-treated aging rats. Finally, the effect of AK-7 on dopaminergic neurons and redox imbalance was supported by the results from primary mesencephalic cultures. Our study helps to elucidate the mechanism for the participation of aging in PD and suggests that SN SIRT2 may be involved in PD neurodegeneration, that AK-7 may be neuroprotective in PD, and that maintaining redox balance may be one of the mechanisms underlying neuroprotection by AK-7. Keywords: Parkinson’s disease, environmental toxin, dopamine, oxidative stress, sirtuin

  8. Do cognitive deficits predict negative emotionality and aggression in schizophrenia?

    Science.gov (United States)

    Ahmed, Anthony O; Richardson, Jenae; Buckner, Alex; Romanoff, Sabrina; Feder, Michelle; Oragunye, Njideka; Ilnicki, Andriana; Bhat, Ishrat; Hoptman, Matthew J; Lindenmayer, Jean-Pierre

    2018-01-01

    Schizophrenia is associated with an elevated risk of aggression. Cognitive deficits have been associated with inpatient aggression and future violence. The relationship between cognitive deficits and violent behavior has however been inconsistent across studies. In addition, studies have failed to inform how cognitive deficits may contribute to aggression in schizophrenia. The current study examined the association of cognitive deficits with schizophrenia-related aggression and violent offending. It also explored the putative mediating role of negative emotionality on the impact of cognitive deficits on aggression. People with schizophrenia and schizoaffective disorder (N = 78) were recruited from a state hospital. Participants were classified based on their history of violent offending. Participants completed measures of cognition, symptoms, and aggression. Deficits in working memory, reasoning/problem-solving, and verbal learning were the most prioritized for the prediction of violent offender status. Violent offenders demonstrated greater impairments in most cognitive domains especially working memory and verbal learning. Offenders also demonstrated greater negative emotionality, excitement/agitation, and incidents of verbal and physical aggression. Negative emotionality and excitement/agitation fully transmitted the effect of cognitive deficits on impulsive aggression in meditational models. Cognitive deficits increase the risk of impulsive aggression in schizophrenia via inefficient regulation of negative affective states. Copyright © 2017 Elsevier B.V. All rights reserved.

  9. A heuristic model for working memory deficit in schizophrenia.

    Science.gov (United States)

    Qi, Zhen; Yu, Gina P; Tretter, Felix; Pogarell, Oliver; Grace, Anthony A; Voit, Eberhard O

    2016-11-01

    The life of schizophrenia patients is severely affected by deficits in working memory. In various brain regions, the reciprocal interactions between excitatory glutamatergic neurons and inhibitory GABAergic neurons are crucial. Other neurotransmitters, in particular dopamine, serotonin, acetylcholine, and norepinephrine, modulate the local balance between glutamate and GABA and therefore regulate the function of brain regions. Persistent alterations in the balances between the neurotransmitters can result in working memory deficits. Here we present a heuristic computational model that accounts for interactions among neurotransmitters across various brain regions. The model is based on the concept of a neurochemical interaction matrix at the biochemical level and combines this matrix with a mobile model representing physiological dynamic balances among neurotransmitter systems associated with working memory. The comparison of clinical and simulation results demonstrates that the model output is qualitatively very consistent with the available data. In addition, the model captured how perturbations migrated through different neurotransmitters and brain regions. Results showed that chronic administration of ketamine can cause a variety of imbalances, and application of an antagonist of the D2 receptor in PFC can also induce imbalances but in a very different manner. The heuristic computational model permits a variety of assessments of genetic, biochemical, and pharmacological perturbations and serves as an intuitive tool for explaining clinical and biological observations. The heuristic model is more intuitive than biophysically detailed models. It can serve as an important tool for interdisciplinary communication and even for psychiatric education of patients and relatives. This article is part of a Special Issue entitled "System Genetics" Guest Editor: Dr. Yudong Cai and Dr. Tao Huang. Copyright © 2016 Elsevier B.V. All rights reserved.

  10. Interferon-gamma deficiency modifies the motor and co-morbid behavioral pathology and neurochemical changes provoked by the pesticide paraquat.

    Science.gov (United States)

    Litteljohn, D; Mangano, E; Shukla, N; Hayley, S

    2009-12-29

    In addition to nigrostriatal pathology and corresponding motor disturbances, Parkinson's disease (PD) is often characterized by co-morbid neuropsychiatric symptoms, most notably anxiety and depression. Separate lines of evidence indicate that inflammatory processes associated with microglial activation and cytokine release may be fundamental to the progression of both PD and its co-morbid psychiatric pathology. Accordingly, we assessed the contribution of the pro-inflammatory cytokine, interferon-gamma (IFN-gamma), to a range of PD-like pathology provoked by the ecologically relevant herbicide and dopamine (DA) toxin, paraquat. To this end, paraquat provoked overt motor impairment (reduced home-cage activity and impaired vertical climbing) and signs of anxiety-like behavior (reduced open field exploration) in wild-type but not IFN-gamma-deficient mice. Correspondingly, paraquat promoted somewhat divergent variations in neurochemical activity among wild-type and IFN-gamma null mice at brain sites important for both motor (striatum) and co-morbid affective pathologies (dorsal hippocampus, medial prefrontal cortex, and locus coeruleus). Specifically, the herbicide provoked a dosing regimen-dependent reduction in striatal DA levels that was prevented by IFN-gamma deficiency. In addition, the herbicide influenced serotonergic and noradrenergic activity within the dorsal hippocampus and medial prefrontal cortex; and elevated noradrenergic activity within the locus coeruleus. Although genetic ablation of IFN-gamma had relatively few effects on monoamine variations within the locus coeruleus and prefrontal cortex, loss of the pro-inflammatory cytokine did normalize the paraquat-induced noradrenergic alterations within the hippocampus. These findings further elucidate the functional implications of paraquat intoxication and suggest an important role for IFN-gamma in the striatal and motor pathology, as well as the co-morbid behavioral and hippocampal changes induced by

  11. A review of the pathophysiology, etiology, and treatment of attention-deficit hyperactivity disorder (ADHD).

    Science.gov (United States)

    Sharma, Alok; Couture, Justin

    2014-02-01

    To review the pathophysiology, etiology, and treatment of attention-deficit hyperactivity disorder (ADHD). A literature search was conducted in PubMed and EMBASE using the terms attention deficit hyperactive disorder, ADHD, pathophysiology, etiology, and neurobiology. Limits applied were the following: published in the past 10 years (January 2003 to August 2013), humans, review, meta-analysis, and English language. These yielded 63 articles in PubMed and 74 in EMBASE. After removing duplicate/irrelevant articles, 86 articles and their relevant reference citations were reviewed. ADHD is a neurological disorder that affects children, but symptoms may persist into adulthood. Individuals suffering from this disorder exhibit hyperactivity, inattention, impulsivity, and problems in social interaction and academic performance. Medications used to treat ADHD such as methylphenidate, amphetamine, and atomoxetine indicate a dopamine/norepinephrine deficit as the neurochemical basis of ADHD, but the etiology is more complex. Moreover, these agents have poor adverse effect profiles and a multitude of drug interactions. Because these drugs are also dispensed to adults who may have concomitant conditions or medications, a pharmacist needs to be aware of these adverse events and drug interactions. This review, therefore, focuses on the pathophysiology, etiology, and treatment of ADHD and details the adverse effects and drug interaction profiles of the drugs used to treat it. Published research shows the benefit of drug therapy for ADHD in children, but given the poor adverse effect and drug interaction profiles, these must be dispensed with caution.

  12. Primary empathy deficits in frontotemporal dementia

    Science.gov (United States)

    Baez, Sandra; Manes, Facundo; Huepe, David; Torralva, Teresa; Fiorentino, Natalia; Richter, Fabian; Huepe-Artigas, Daniela; Ferrari, Jesica; Montañes, Patricia; Reyes, Pablo; Matallana, Diana; Vigliecca, Nora S.; Decety, Jean; Ibanez, Agustin

    2014-01-01

    Loss of empathy is an early central symptom and diagnostic criterion of the behavioral variant frontotemporal dementia (bvFTD). Although changes in empathy are evident and strongly affect the social functioning of bvFTD patients, few studies have directly investigated this issue by means of experimental paradigms. The current study assessed multiple components of empathy (affective, cognitive and moral) in bvFTD patients. We also explored whether the loss of empathy constitutes a primary deficit of bvFTD or whether it is explained by impairments in executive functions (EF) or other social cognition domains. Thirty-seven bvFTD patients with early/mild stages of the disease and 30 healthy control participants were assessed with a task that involves the perception of intentional and accidental harm. Participants were also evaluated on emotion recognition, theory of mind (ToM), social norms knowledge and several EF domains. BvFTD patients presented deficits in affective, cognitive and moral aspects of empathy. However, empathic concern was the only aspect primarily affected in bvFTD that was neither related nor explained by deficits in EF or other social cognition domains. Deficits in the cognitive and moral aspects of empathy seem to depend on EF, emotion recognition and ToM. Our findings highlight the importance of using tasks depicting real-life social scenarios because of their greater sensitivity in the assessment of bvFTD. Moreover, our results contribute to the understanding of primary and intrinsic empathy deficits of bvFTD and have important theoretical and clinical implications. PMID:25346685

  13. Working and strategic memory deficits in schizophrenia

    Science.gov (United States)

    Stone, M.; Gabrieli, J. D.; Stebbins, G. T.; Sullivan, E. V.

    1998-01-01

    Working memory and its contribution to performance on strategic memory tests in schizophrenia were studied. Patients (n = 18) and control participants (n = 15), all men, received tests of immediate memory (forward digit span), working memory (listening, computation, and backward digit span), and long-term strategic (free recall, temporal order, and self-ordered pointing) and nonstrategic (recognition) memory. Schizophrenia patients performed worse on all tests. Education, verbal intelligence, and immediate memory capacity did not account for deficits in working memory in schizophrenia patients. Reduced working memory capacity accounted for group differences in strategic memory but not in recognition memory. Working memory impairment may be central to the profile of impaired cognitive performance in schizophrenia and is consistent with hypothesized frontal lobe dysfunction associated with this disease. Additional medial-temporal dysfunction may account for the recognition memory deficit.

  14. In science communication, why does the idea of the public deficit always return? Exploring key influences.

    Science.gov (United States)

    Suldovsky, Brianne

    2016-05-01

    Despite mounting criticism, the deficit model remains an integral part of science communication research and practice. In this article, I advance three key factors that contribute to the idea of the public deficit in science communication, including the purpose of science communication, how communication processes and outcomes are conceptualized, and how science and scientific knowledge are defined. Affording science absolute epistemic privilege, I argue, is the most compelling factor contributing to the continued use of the deficit model. In addition, I contend that the deficit model plays a necessary, though not sufficient, role in science communication research and practice. Areas for future research are discussed. © The Author(s) 2016.

  15. How semantic deficits in schizotypy help understand language and thought disorders in schizophrenia: a systematic and integrative review

    Directory of Open Access Journals (Sweden)

    Hélio Anderson Tonelli

    2014-04-01

    Full Text Available Introduction: Disorders of thought are psychopathological phenomena commonly present in schizophrenia and seem to result from deficits of semantic processing. Schizotypal personality traits consist of tendencies to think and behave that are qualitatively similar to schizophrenia, with greater vulnerability to such disorder. This study reviewed the literature about semantic processing deficits in samples of individuals with schizotypal traits and discussed the impact of current knowledge upon the comprehension of schizophrenic thought disorders. Studies about the cognitive performance of healthy individuals with schizotypal traits help understand the semantic deficits underlying psychotic thought disorders with the advantage of avoiding confounding factors usually found in samples of individuals with schizophrenia, such as the use of antipsychotics and hospitalizations. Methods: A search for articles published in Portuguese or English within the last 10 years on the databases MEDLINE, Web of Science, PsycInfo, LILACS and Biological Abstracts was conducted, using the keywords semantic processing, schizotypy and schizotypal personality disorder. Results: The search retrieved 44 manuscripts, out of which 11 were firstly chosen. Seven manuscripts were additionally included after reading these papers. Conclusion: The great majority of the included studies showed that schizotypal subjects might exhibit semantic processing deficits. They help clarify about the interfaces between cognitive, neurophysiological and neurochemical mechanisms underlying not only thought disorders, but also healthy human mind's creativity.

  16. Protective effect of curcumin and its combination with piperine (bioavailability enhancer) against haloperidol-associated neurotoxicity: cellular and neurochemical evidence.

    Science.gov (United States)

    Bishnoi, Mahendra; Chopra, Kanwaljit; Rongzhu, Lu; Kulkarni, Shrinivas K

    2011-10-01

    Long-term treatment with haloperidol is associated with a number of extrapyramidal side effects, particularly the irregular movements of chorionic type. This limitation presents a marked therapeutic challenge. The present study investigates the molecular etiology of haloperidol neurotoxicity and the role of curcumin, a well-known anti-oxidant, in ameliorating these adverse effects. The redox status of haloperidol-treated brains along with NO, TNF-α, NF-kappaB p65 subunit, caspase-3, and monoamine neurotransmitters were measured in the striatum of rat brain. Chronic treatment with haloperidol (5 mg/kg, i.p., 21 days) produced orofacial dyskinetic movements which were coupled with marked increase in oxidative stress parameters, TNF-α, caspase-3 activity in cytoplasmic lysate and active p65 sub unit of NF-kappaB in nuclear lysates of the striatum. Neurochemically, chronic administration of haloperidol resulted in a significant decrease in the levels of norepinephrine, dopamine, and serotonin. The prototype atypical anti-psychotic, clozapine (10 mg/kg, i.p., 21 days) produced mild oxidative stress but did not alter any other parameters. Interestingly, co-administration of curcumin (25 and 50 mg/kg, i.p., 21 days) dose-dependently prevented all the behavioral, cellular, and neurochemical changes associated with the chronic administration of haloperidol. Curcumin per se (50 mg/kg) did not show any side effects. Co-administration of piperine significantly enhanced the effect of curcumin (25 mg/kg) but not of curcumin (50 mg/kg). Collectively, the data indicated the potential of curcumin as an adjunct to haloperidol treatment and provided initial clues to the underlying molecular mechanisms in haloperidol neurotoxicity. This study also provides a rationale for the combination of piperine and curcumin.

  17. Effects of electroconvulsive seizures on depression-related behavior, memory and neurochemical changes in Wistar and Wistar-Kyoto rats.

    Science.gov (United States)

    Kyeremanteng, C; MacKay, J C; James, J S; Kent, P; Cayer, C; Anisman, H; Merali, Z

    2014-10-03

    Investigations in healthy outbred rat strains have shown a potential role for brain-derived neurotrophic factor (BDNF) and the hypothalamic-pituitary-adrenal (HPA) axis in the antidepressant and memory side effects of electroconvulsive therapy (ECT, or ECS in animals). The Wistar-Kyoto (WKY) rat strain is used as a genetic model of depression yet no studies to date have directly compared the impact of ECS on the WKY strain to its healthy outbred control (Wistar). The objective of this study is to examine behavioral (antidepressant and retrograde memory) and neurochemical (BDNF and HPA axis) changes immediately (1day) and at a longer delay (7days) after repeated ECS (5 daily administrations) in WKY and Wistar rats. Male Wistar and WKY rats received 5days of repeated ECS or sham treatment and were assessed 1 and 7days later for 1) depression-like behavior and mobility; 2) retrograde memory; and 3) brain BDNF protein, brain corticotropin-releasing factor (CRF) and plasma corticosterone levels. Both strains showed the expected antidepressant response and retrograde memory impairments at 1day following ECS, which were sustained at 7days. In addition, at 1day after ECS, Wistar and WKY rats showed similar elevations in brain BDNF and extra-hypothalamic CRF and no change in plasma corticosterone. At 7days after ECS, Wistar rats showed sustained elevations of brain BDNF and CRF, whereas WKY rats showed a normalization of brain BDNF, despite sustained elevations of brain CRF. The model of 5 daily ECS was effective at eliciting behavioral and neurochemical changes in both strains. A temporal association was observed between brain CRF levels, but not BDNF, and measures of antidepressant effectiveness of ECS and retrograde memory impairments suggesting that extra-hypothalamic CRF may be a potential important contributor to these behavioral effects after repeated ECS/ECT. Copyright © 2014 Elsevier Inc. All rights reserved.

  18. Impulsivity and verbal deficits associated with domestic violence.

    Science.gov (United States)

    Cohen, Ronald A; Brumm, Virdette; Zawacki, Tricia M; Paul, Robert; Sweet, Lawrence; Rosenbaum, Alan

    2003-07-01

    While neurobiological factors are known to play a role in human aggression, relatively few studies have examined neuropsychological contributions to propensity for violence. We previously demonstrated cognitive deficits among men who committed domestic violence (batterers) compared to non-violent controls. Batterers had deficits in verbal ability, learning and executive problem-solving ability. These findings led us to examine whether executive control problems involving impulsivity contribute to problems with behavioral control among batterers, and to further examine their deficits in verbal functioning. Batterers (n = 41) enrolled in a domestic violence program were compared to 20 non-violent men of similar age, education, and socioeconomic background on neuropsychological tests of executive functioning, including impulsivity. Questionnaires and structured clinical interviews were used to assess emotional distress, aggression and self-reported impulsivity. Batterers showed greater impulsivity compared to non-batterers on several neuropsychological measures. Yet, the severity of these deficits was relatively mild and not evident in all batterers. Consistent with our previous findings, significant verbal deficits were again observed among the batterers. These findings suggest that while impulsivity may be a factor associated with domestic violence, it probably is not the sole determinant of the strong relationship between cognitive functioning and batterer status that we previously observed. Both verbal expressive deficits and behavioral impulsivity appear to be relevant variables in predisposing men to domestic violence.

  19. Attention Deficit Hyperactivity Disorder

    Science.gov (United States)

    Matthews, Marguerite; Nigg, Joel T.

    2014-01-01

    Over the last two decades, there have been numerous technical and methodological advances available to clinicians and researchers to better understand attention deficit hyperactivity disorder (ADHD) and its etiology. Despite the growing body of literature investigating the disorder’s pathophysiology, ADHD remains a complex psychiatric disorder to characterize. This chapter will briefly review the literature on ADHD, with a focus on its history, the current genetic insights, neurophysiologic theories, and the use of neuroimaging to further understand the etiology. We address some of the major concerns that remain unclear about ADHD, including subtype instability, heterogeneity, and the underlying neural correlates that define the disorder. We highlight that the field of ADHD is rapidly evolving; the descriptions provided here will hopefully provide a sturdy foundation for which to build and improve our understanding of the disorder. PMID:24214656

  20. Neurobehavioral Deficits in Progressive Experimental ...

    African Journals Online (AJOL)

    olayemitoyin

    Departments of 1Anatomy and 2Neurological Surgery, College of Medicine, University of Ibadan, Nigeria. Summary: Hydrocephalus is usually associated with functional deficits which can be assessed by neurobehavioral tests. This study characterizes the neurobehavioral deficits occurring with increasing duration and ...

  1. Dyscalculia and Attention Deficit Subtypes

    OpenAIRE

    J Gordon Millichap

    1999-01-01

    The association of specific academic deficits with attention deficit disorder (ADD) subtypes was determined in 20 students (ages 8-12) with ADD with hyperactivity (ADD/H) compared to 20 with ADD without hyperactivity (ADD/noH), at the Department of Educational Psychology, University of Texas at Austin, TX.

  2. Pragmatic communication deficits in children with epilepsy

    NARCIS (Netherlands)

    Broeders, Mark; Geurts, Hilde; Jennekens-Schinkel, Aag

    2010-01-01

    Background: Various psychiatric and neurological disorders including epilepsy have been associated with language deficits. Pragmatic language deficits, however, have seldom been the focus of earlier studies in children with epilepsy. Moreover, it is unknown whether these pragmatic deficits are

  3. [Attention deficit hyperactivity disorder].

    Science.gov (United States)

    Cunill, Ruth; Castells, Xavier

    2015-04-20

    Attention deficit hyperactivity disorder (ADHD) is one of the most common childhood psychiatric disorders and can persist into the adulthood. ADHD has important social, academic and occupational consequences. ADHD diagnosis is based on the fulfillment of several clinical criteria, which can vary depending on the diagnostic system used. The clinical presentation can show great between-patient variability and it has been related to a dysfunction in the fronto-striatal and meso-limbic circuits. Recent investigations support a model in which multiple genetic and environmental factors interact to create a neurobiological susceptibility to develop the disorder. However, no clear causal association has yet been identified. Although multimodal treatment including both pharmacological and psychosocial interventions is usually recommended, no convincing evidence exists to support this recommendation. Pharmacological treatment has fundamentally shown to improve ADHD symptoms in the short term, while efficacy data for psychosocial interventions are scarce and inconsistent. Yet, drug treatment is increasingly popular and the last 2 decades have witnessed a sharp increase in the prescription of anti-ADHD medications coinciding with the marketing of new drugs to treat ADHD. Copyright © 2014 Elsevier España, S.L.U. All rights reserved.

  4. Prefrontal activation deficits during episodic memory in schizophrenia.

    Science.gov (United States)

    Ragland, John D; Laird, Angela R; Ranganath, Charan; Blumenfeld, Robert S; Gonzales, Sabina M; Glahn, David C

    2009-08-01

    Episodic memory impairments represent a core deficit in schizophrenia that severely limits patients' functional outcome. This quantitative meta-analysis of functional imaging studies of episodic encoding and retrieval tests the prediction that these deficits are most consistently associated with dysfunction in the prefrontal cortex. Activation likelihood estimation (ALE) was used to perform a quantitative meta-analysis of functional imaging studies that contrasted patients with schizophrenia and healthy volunteers during episodic encoding and retrieval. From a pool of 36 potential studies, 18 whole-brain studies in standard space that included a healthy comparison sample and low-level baseline contrast were selected. As predicted, patients showed less prefrontal activation than comparison subjects in the frontal pole, dorsolateral and ventrolateral prefrontal cortex during encoding, and the dorsolateral prefrontal cortex and ventrolateral prefrontal cortex during retrieval. The ventrolateral prefrontal cortex encoding deficits were not present in studies that provided patients with encoding strategies, but dorsolateral prefrontal cortex deficits remained and were not secondary to group performance differences. The only medial temporal lobe finding was relatively greater patient versus comparison subject activation in the parahippocampal gyrus during encoding and retrieval. The finding of prominent prefrontal dysfunction suggests that cognitive control deficits strongly contribute to episodic memory impairment in schizophrenia. Memory rehabilitation approaches developed for patients with frontal lobe lesions and pharmacotherapy approaches designed to improve prefrontal cortex function may therefore hold special promise for remediating memory deficits in patients with schizophrenia.

  5. Adult attention-deficit hyperactivity disorder: Why should we pay ...

    African Journals Online (AJOL)

    Background: Attention-deficit hyperactivity disorder (ADHD) is a common neurodevelopmental disorder, with a chronic, costly and debilitating course if untreated. Limited access to diagnosis and treatment for adults with ADHD contributes to the cost of the disorder and the burden of disease. Aim: This study aims to identify ...

  6. Sustaining smallholder farmers' livelihoods through rainfall-deficit ...

    African Journals Online (AJOL)

    The main objective of this article is to assess the contributions in sustaining the livelihoods of smallholder farmers of rainfall-deficit-index-based crop insurance pilot project based on haricot beans implemented in Ethiopia in 2009. Based on crosssectional data, assessment results revealed that crop insurance has a ...

  7. Developmental Dyslexia: The Visual Attention Span Deficit Hypothesis

    Science.gov (United States)

    Bosse, Marie-Line; Tainturier, Marie Josephe; Valdois, Sylviane

    2007-01-01

    The visual attention (VA) span is defined as the amount of distinct visual elements which can be processed in parallel in a multi-element array. Both recent empirical data and theoretical accounts suggest that a VA span deficit might contribute to developmental dyslexia, independently of a phonological disorder. In this study, this hypothesis was…

  8. Attention Deficit Hyperactivity Disorder (ADHD)

    Science.gov (United States)

    ... NIH About Mission The NIH Director Organization Budget History NIH Almanac Public Involvement Outreach & Education Visitor Information RePORT NIH Fact Sheets Home > Attention Deficit Hyperactivity Disorder (ADHD) Small Text Medium Text Large Text ...

  9. Functional Circuitry Effect of Ventral Tegmental Area Deep Brain Stimulation: Imaging and Neurochemical Evidence of Mesocortical and Mesolimbic Pathway Modulation.

    Science.gov (United States)

    Settell, Megan L; Testini, Paola; Cho, Shinho; Lee, Jannifer H; Blaha, Charles D; Jo, Hang J; Lee, Kendall H; Min, Hoon-Ki

    2017-01-01

    Background: The ventral tegmental area (VTA), containing mesolimbic and mesocortical dopaminergic neurons, is implicated in processes involving reward, addiction, reinforcement, and learning, which are associated with a variety of neuropsychiatric disorders. Electrical stimulation of the VTA or the medial forebrain bundle and its projection target the nucleus accumbens (NAc) is reported to improve depressive symptoms in patients affected by severe, treatment-resistant major depressive disorder (MDD) and depressive-like symptoms in animal models of depression. Here we sought to determine the neuromodulatory effects of VTA deep brain stimulation (DBS) in a normal large animal model (swine) by combining neurochemical measurements with functional magnetic resonance imaging (fMRI). Methods: Animals (n = 8 swine) were implanted with a unilateral DBS electrode targeting the VTA. During stimulation (130 Hz frequency, 0.25 ms pulse width, and 3 V amplitude), fMRI was performed. Following fMRI, fast-scan cyclic voltammetry in combination with carbon fiber microelectrodes was performed to quantify VTA-DBS-evoked dopamine release in the ipsilateral NAc. In a subset of swine, the blood oxygen level-dependent (BOLD) percent change evoked by stimulation was performed at increasing voltages (1, 2, and 3 V). Results: A significant increase in VTA-DBS-evoked BOLD signal was found in the following regions: the ipsilateral dorsolateral prefrontal cortex, anterior and posterior cingulate, insula, premotor cortex, primary somatosensory cortex, and striatum. A decrease in the BOLD signal was also observed in the contralateral parahippocampal cortex, dorsolateral and anterior prefrontal cortex, insula, inferior temporal gyrus, and primary somatosensory cortex (Bonferroni-corrected modulation of the neural circuitry associated with VTA-DBS was characterized in a large animal. Our findings suggest that VTA-DBS could affect the activity of neural systems and brain regions implicated in

  10. Transplacental exposure to AZT induces adverse neurochemical and behavioral effects in a mouse model: protection by L-acetylcarnitine.

    Directory of Open Access Journals (Sweden)

    Anna Rita Zuena

    Full Text Available Maternal-fetal HIV-1 transmission can be prevented by administration of AZT, alone or in combination with other antiretroviral drugs to pregnant HIV-1-infected women and their newborns. In spite of the benefits deriving from this life-saving prophylactic therapy, there is still considerable uncertainty on the potential long-term adverse effects of antiretroviral drugs on exposed children. Clinical and experimental studies have consistently shown the occurrence of mitochondrial dysfunction and increased oxidative stress following prenatal treatment with antiretroviral drugs, and clinical evidence suggests that the developing brain is one of the targets of the toxic action of these compounds possibly resulting in behavioral problems. We intended to verify the effects on brain and behavior of mice exposed during gestation to AZT, the backbone of antiretroviral therapy during human pregnancy. We hypothesized that glutamate, a neurotransmitter involved in excitotoxicity and behavioral plasticity, could be one of the major actors in AZT-induced neurochemical and behavioral alterations. We also assessed the antioxidant and neuroprotective effect of L-acetylcarnitine, a compound that improves mitochondrial function and is successfully used to treat antiretroviral-induced polyneuropathy in HIV-1 patients. We found that transplacental exposure to AZT given per os to pregnant mice from day 10 of pregnancy to delivery impaired in the adult offspring spatial learning and memory, enhanced corticosterone release in response to acute stress, increased brain oxidative stress also at birth and markedly reduced expression of mGluR1 and mGluR5 subtypes and GluR1 subunit of AMPA receptors in the hippocampus. Notably, administration during the entire pregnancy of L-acetylcarnitine was effective in preventing/ameliorating the neurochemical, neuroendocrine and behavioral adverse effects induced by AZT in the offspring. The present preclinical findings provide a

  11. Budget deficits and public debt

    OpenAIRE

    Ph.D. Student Ionut Constantin

    2009-01-01

    In the recent decades, the budget deficit has become one of the characteristics of national economies. Furthermore, it finds its dimensions amplification. Despite this, more and more are the economists who dispute the need to balance the budget, arguing the need even the deficit and systematic use of in order to achieve economic equilibrium. Such guidance is substantiated by the need to promote an economic policy which ensures full use of resources and non-inflation economic growth.In these c...

  12. Neurochemical and behavioral indices of exercise reward are independent of exercise controllability

    OpenAIRE

    Herrera, Jonathan J.; Fedynska, Sofiya; Ghasem, Parsa R; Wieman, Tyler; Clark, Peter J.; Gray, Nathan; Loetz, Esteban; Campeau, Serge; Fleshner, Monika; Greenwood, Benjamin N.

    2016-01-01

    Brain reward circuits are implicated in stress-related psychiatric disorders. Exercise reduces the incidence of stress-related disorders, but the contribution of exercise reward to stress resistance is unknown. Exercise-induced stress resistance is independent of exercise controllability; both voluntary and forced wheel running protect rats against anxiety- and depression-like behavioral consequences of stress. Voluntary exercise is a natural reward, but whether rats find forced wheel running...

  13. Magnesium treatment palliates noise-induced behavioral deficits by normalizing DAergic and 5-HTergic metabolism in adult male rats.

    Science.gov (United States)

    Haider, Saida; Sadir, Sadia; Naqvi, Fizza; Batool, Zehra; Tabassum, Saiqa; Khaliq, Saima; Anis, Lubna; Sajid, Irfan; Haleem, Darakhshan J

    2016-08-01

    Magnesium (Mg) is the fourth most abundant biological mineral essential for good health. Neuroprotective, anxiolytic and antidepressant effects of magnesium following stress and brain injuries are well established. In present study, we analyzed the protective effects of magnesium in rats exposed to sub-chronic noise stress. Magnesium Chloride (MgCl2, 100 mg/kg) was administered intraperitoneally once daily for 15 days prior exposure to noise stress. Rats were exposed to noise stress for 4 h after administration of magnesium for 15 days. At the end of treatment behavioral alterations were assessed. Animals were decapitated following behavioral testing and the brains were dissected out for neurochemical estimations by HPLC-EC. Improvement in noise-induced memory deficits as assessed by novel object recognition (NOR) test and elevated plus maze (EPM) test was found in magnesium treated rats. This improvement in noise-induced behavioral deficits following treatment with magnesium may be attributed to a significant decrease (p < 0.01) in dopamine (DA) and serotonin (5-hydroxytryptamine; 5-HT) turnover as compared to control rats observed in present work. These results suggest that treatment with magnesium can attenuate the noise-induced deficits and may be used as a therapy against noise-induced neurodegeneration. Moreover an adequate amount of magnesium in daily diet may help to develop the ability to resist against or cope up with stressful conditions encountered in daily life.

  14. Theophylline, adenosine receptor antagonist prevents behavioral, biochemical and neurochemical changes associated with an animal model of tardive dyskinesia.

    Science.gov (United States)

    Bishnoi, Mahendra; Chopra, Kanwaljit; Kulkarni, Shrinivas K

    2007-01-01

    Tardive dyskinesia is considered to be the late onset adverse effect of prolonged administration of typical neuroleptic drugs. Adenosine is now widely accepted as the major inhibitory neuromodulators in the central nervous system besides GABA. Antagonists of A2A receptors are known to confer protection against neuronal damage caused by toxins and reactive oxygen species. The present study investigated the effect of adenosine receptor antagonist, theophylline (25 and 50 mg/kg, ip) in an animal model of tardive dyskinesia by using different behavioral (orofacial dyskinetic movements, stereotypy, locomotor activity, % retention), biochemical (lipid peroxidation, reduced glutathione levels, antioxidant enzyme levels (SOD and catalase)) and neurochemical (neurotransmitter levels) parameters. Chronic administration of haloperidol (1 mg/kg ip for 21 days) significantly increased vacuous chewing movements (VCMs), tongue protrusions, facial jerking in rats which was dose-dependently inhibited by theophylline. Chronic administration of haloperidol also resulted in the increased dopamine receptor sensitivity as evidenced by increased locomotor activity and stereotypic rearing. Further, it also decreased % retention time in elevated plus maze paradigm. Pretreatment with theophylline reversed these behavioral changes. Chronic administration of haloperidol also induced oxidative damage in all the brain regions which was prevented by theophylline, especially in the striatum. Chronic administration of haloperidol resulted in a decrease in dopamine levels which was reversed by treatment with theophylline (at higher doses). The findings of the present study suggested the involvement of adenosinergic receptor system in the development of tardive dyskinesia and possible therapeutic potential of theophylline in this disorder.

  15. Functional and neurochemical interactions within the amygdala-medial prefrontal cortex circuit and their relevance to emotional processing.

    Science.gov (United States)

    Delli Pizzi, Stefano; Chiacchiaretta, Piero; Mantini, Dante; Bubbico, Giovanna; Ferretti, Antonio; Edden, Richard A; Di Giulio, Camillo; Onofrj, Marco; Bonanni, Laura

    2017-04-01

    The amygdala-medial prefrontal cortex (mPFC) circuit plays a key role in emotional processing. GABA-ergic inhibition within the mPFC has been suggested to play a role in the shaping of amygdala activity. However, the functional and neurochemical interactions within the amygdala-mPFC circuits and their relevance to emotional processing remain unclear. To investigate this circuit, we obtained resting-state functional magnetic resonance imaging (rs-fMRI) and proton MR spectroscopy in 21 healthy subjects to assess the potential relationship between GABA levels within mPFC and the amygdala-mPFC functional connectivity. Trait anxiety was assessed using the State-Trait Anxiety Inventory (STAI-Y2). Partial correlations were used to measure the relationships among the functional connectivity outcomes, mPFC GABA levels and STAI-Y2 scores. Age, educational level and amount of the gray and white matters within 1 H-MRS volume of interest were included as nuisance variables. The rs-fMRI signals of the amygdala and the vmPFC were significantly anti-correlated. This negative functional coupling between the two regions was inversely correlated with the GABA+/tCr level within the mPFC and the STAI-Y2 scores. We suggest a close relationship between mPFC GABA levels and functional interactions within the amygdala-vmPFC circuit, providing new insights in the physiology of emotion.

  16. Magnesium Sulfate Prevents Neurochemical and Long-Term Behavioral Consequences of Neonatal Excitotoxic Lesions: Comparison Between Male and Female Mice.

    Science.gov (United States)

    Daher, Ismaël; Le Dieu-Lugon, Bérénice; Dourmap, Nathalie; Lecuyer, Matthieu; Ramet, Lauriane; Gomila, Cathy; Ausseil, Jérôme; Marret, Stéphane; Leroux, Philippe; Roy, Vincent; El Mestikawy, Salah; Daumas, Stéphanie; Gonzalez, Bruno; Leroux-Nicollet, Isabelle; Cleren, Carine

    2017-10-01

    Magnesium sulfate (MgSO4) administration to mothers at risk of preterm delivery is proposed as a neuroprotective strategy against neurological alterations such as cerebral palsy in newborns. However, long-term beneficial or adverse effects of MgSO4 and sex-specific sensitivity remain to be investigated. We conducted behavioral and neurochemical studies of MgSO4 effects in males and females, from the perinatal period to adolescence in a mouse model of cerebral neonatal lesion. The lesion was produced in 5-day-old (P5) pups by ibotenate intracortical injection. MgSO4 (600 mg/kg, i.p.) prior to ibotenate prevented lesion-induced sensorimotor alterations in both sexes at P6 and P7. The lesion increased glutamate level at P10 in the prefrontal cortex, which was prevented by MgSO4 in males. In neonatally lesioned adolescent mice, males exhibited more sequelae than females in motor and cognitive functions. In the perirhinal cortex of adolescent mice, the neonatal lesion induced an increase in vesicular glutamate transporter 1 density in males only, which was negatively correlated with cognitive scores. Long-term sequelae were prevented by neonatal MgSO4 administration. MgSO4 never induced short- or long-term deleterious effect on its own. These results also strongly suggest that sex-specific neuroprotection should be foreseen in preterm infants. © 2017 American Association of Neuropathologists, Inc. All rights reserved.

  17. PRAGMATIC DEFICITS OF ASPERGER SYNDROME

    Directory of Open Access Journals (Sweden)

    Silmy Arizatul Humaira’

    2015-08-01

    Full Text Available Human being is social creature who needs other people to interact with. One of the ways to interact with others is communication with language. However, communication could be a complicated problem for those who were born with developmental disorder called Asperger Syndrome (AS. The communication challenge of Asperger’s is the difficulty using language appropriately for social purposes or known as pragmatic deficits. Many excellent books about autism are published whereas knowledge on pragmatic deficits are still very limited. Thus, it is expected to be a beneficial reference to understand the pragmatic deficits and to create strategies for them to communicate effectively. Therefore, this study aimed at exploring the kinds of pragmatic deficits of an individual with AS. The verbal language profiles of autism purposed by MacDonald (2004 is used to analyzed the data in depth. The descriptive qualitative method is applied to develop a comprehensive understanding about the AS case in Temple Grandin movie.The finding shows that all of the five types of communication deficits are appearing and the dominant of which is unresponsive.

  18. Neurochemical and behavioral indices of exercise reward are independent of exercise controllability

    Science.gov (United States)

    Herrera, Jonathan J; Fedynska, Sofiya; Ghasem, Parsa R; Wieman, Tyler; Clark, Peter J; Gray, Nathan; Loetz, Esteban; Campeau, Serge; Fleshner, Monika; Greenwood, Benjamin N

    2016-01-01

    Brain reward circuits are implicated in stress-related psychiatric disorders. Exercise reduces the incidence of stress-related disorders, but the contribution of exercise reward to stress resistance is unknown. Exercise-induced stress resistance is independent of exercise controllability; both voluntary and forced wheel running protect rats against anxiety- and depression-like behavioral consequences of stress. Voluntary exercise is a natural reward, but whether rats find forced wheel running rewarding is unknown. Moreover, the contribution of dopamine (DA) and striatal reward circuits to exercise reward is not well characterized. Adult, male rats were assigned to locked wheels, voluntary running (VR), or forced running (FR) groups. FR rats were forced to run in a pattern resembling rats' natural wheel running behavior. Both VR and FR increased the reward-related plasticity marker ΔFosB in the dorsal striatum (DS) and nucleus accumbens (NAc), and increased activity of DA neurons in the lateral ventral tegmental area (VTA), as revealed by immunohistochemistry for tyrosine hydroxylase (TH) and pCREB. Both VR and FR rats developed conditioned place preference (CPP) to the side of a CPP chamber paired with exercise. Re-exposure to the exercise-paired side of the CPP chamber elicited conditioned increases in cfos mRNA in direct pathway (dynorphin-positive) neurons in the DS and NAc in both VR and FR rats, and in TH-positive neurons in the lateral VTA of VR rats only. Results suggest that the rewarding effects of exercise are independent of exercise controllability and provide insight into the DA and striatal circuitries involved in exercise reward and exercise-induced stress resistance. PMID:26833814

  19. Neurochemical and behavioural indices of exercise reward are independent of exercise controllability.

    Science.gov (United States)

    Herrera, Jonathan J; Fedynska, Sofiya; Ghasem, Parsa R; Wieman, Tyler; Clark, Peter J; Gray, Nathan; Loetz, Esteban; Campeau, Serge; Fleshner, Monika; Greenwood, Benjamin N

    2016-05-01

    Brain reward circuits are implicated in stress-related psychiatric disorders. Exercise reduces the incidence of stress-related disorders, but the contribution of exercise reward to stress resistance is unknown. Exercise-induced stress resistance is independent of exercise controllability; both voluntary running (VR) and forced running (FR) protect rats against the anxiety-like and depression-like behavioural consequences of stress. Voluntary exercise is a natural reward, but whether rats find FR rewarding is unknown. Moreover, the contribution of dopamine (DA) and striatal reward circuits to exercise reward is not well characterized. Adult, male rats were assigned to locked wheels, VR, or FR groups. FR rats were forced to run in a pattern resembling the natural wheel running behavior of rats. Both VR and FR increased the reward-related plasticity marker ΔFosB in the dorsal striatum and nucleus accumbens, and increased the activity of DA neurons in the lateral ventral tegmental area, as revealed by immunohistochemistry for tyrosine hydroxylase and pCREB. Both VR and FR rats developed conditioned place preference (CPP) to the side of a CPP chamber paired with exercise. Re-exposure to the exercise-paired side of the CPP chamber elicited conditioned increases in cfos mRNA in direct-pathway (dynorphin-positive) neurons in the dorsal striatum and nucleus accumbens in both VR and FR rats, and in tyrosine hydroxylase-positive neurons in the lateral ventral tegmental area of VR rats only. The results suggest that the rewarding effects of exercise are independent of exercise controllability and provide insight into the DA and striatal circuitries involved in exercise reward and exercise-induced stress resistance. © 2016 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.

  20. Restoration of MPTP-induced deficits by exercise and Milmed® co-treatment

    Directory of Open Access Journals (Sweden)

    Trevor Archer

    2014-08-01

    Full Text Available 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP induces permanent neurochemical and functional deficits. Following the administration of either two or four injections of the dopamine neurotoxin, MPTP, at a dose of 40 mg/kg, C57/BL6 mice were given access to running-wheels (30-min sessions, four times/week, Monday–Thursday and treatment with the treated yeast, Milmed® (four times/week, Monday–Thursday, or simply running-wheel exercise by itself, over ten weeks. It was observed that the combination of physical exercise and Milmed® treatment, the MPTP + Exercise + Yeast (MC group [MPTP + Exercise + Milmed® (MC], restored spontaneous motor activity markedly by test day 10, restored completely subthreshold L-Dopa-induced activity, and dopamine concentration to 76% of control values, in the condition wherein two administrations of MPTP (2 × 40 mg/kg were given prior to initiation of exercise and/or Milmed® treatment. Physical exercise by itself, MPTP + Exercise (MC group, attenuated these deficits only partially. Administration of MPTP four times (i.e., 40 mg/kg, s.c., once weekly over four weeks for a total of 160 mg/kg, MPTP + Exercise + Yeast (MC group [MPTP + Exercise + Milmed® (SC] and MPTP + Exercise (SC, induced a lesioning effect that was far too severe for either exercise alone or the exercise + Milmed® combination to ameliorate. Nevertheless, these findings indicate a powerful effect of physical exercise reinforced by Milmed® treatment in restoring MPTP-induced deficits of motor function and dopamine neurochemistry in mice.

  1. CREB Overexpression Ameliorates Age-related Behavioral and Biophysical Deficits

    Science.gov (United States)

    Yu, Xiao-Wen

    Age-related cognitive deficits are observed in both humans and animals. Yet, the molecular mechanisms underlying these deficits are not yet fully elucidated. In aged animals, a decrease in intrinsic excitability of pyramidal neurons from the CA1 sub-region of hippocampus is believed to contribute to age-related cognitive impairments, but the molecular mechanism(s) that modulate both these factors has yet to be identified. Increasing activity of the transcription factor cAMP response element-binding protein (CREB) in young adult rodents has been shown to facilitate cognition, and increase intrinsic excitability of their neurons. However, how CREB changes with age, and how that impacts cognition in aged animals, is not clear. Therefore, we first systematically characterized age- and training-related changes in CREB levels in dorsal hippocampus. At a remote time point after undergoing behavioral training, levels of total CREB and activated CREB (phosphorylated at S133, pCREB) were measured in both young and aged rats. We found that pCREB, but not total CREB was significantly reduced in dorsal CA1 of aged rats. Importantly, levels of pCREB were found to be positively correlated with short-term spatial memory in both young and aged rats i.e. higher pCREB in dorsal CA1 was associated with better spatial memory. These findings indicate that an age-related deficit in CREB activity may contribute to the development of age-related cognitive deficits. However, it was still unclear if increasing CREB activity would be sufficient to ameliorate age-related cognitive, and biophysical deficits. To address this question, we virally overexpressed CREB in CA1, where we found the age-related deficit. Young and aged rats received control or CREB virus, and underwent water maze training. While control aged animals exhibited deficits in long-term spatial memory, aged animals with CREB overexpression performed at levels comparable to young animals. Concurrently, aged neurons

  2. Budget deficits and public debt

    Directory of Open Access Journals (Sweden)

    Ph. D. Student Ionut Constantin

    2009-05-01

    Full Text Available In the recent decades, the budget deficit has become one of the characteristics of national economies. Furthermore, it finds its dimensions amplification. Despite this, more and more are the economists who dispute the need to balance the budget, arguing the need even the deficit and systematic use of in order to achieve economic equilibrium. Such guidance is substantiated by the need to promote an economic policy which ensures full use of resources and non-inflation economic growth.In these circumstances, balancing the budgest is clearly of secondary importance. In this context, it supported the need to increase expenditure at a pace faster than income growth and, implicitly , to keep budget deficits.

  3. Disentangling Early Sensory Information Processing Deficits in Schizophrenia

    Science.gov (United States)

    Rissling, Anthony J.; Braff, David L.; Swerdlow, Neal R.; Hellemann, Gerhard; Rassovsky, Yuri; Sprock, Joyce; Pela, Marlena; Light, Gregory A.

    2012-01-01

    Objective The disentangling of early sensory information processing deficits and examination of their relationships to demographic and clinical factors are important steps for the validation of potential biomarkers and/or endophenotypes of schizophrenia. The aims of the present study were to characterize commonly used sensory event-related potential deficits, to determine whether they are 1) distinct from one another and 2) independently associated with important clinical characteristics. Methods MMN, P3a and RON event-related potentials (ERP) were recorded from schizophrenia patients (SZ; n=429) and nonpsychiatric comparison subjects (NCS; n=286). Subgroup analyses on demographic and clinical variables were performed. Results Schizophrenia patients exhibited robust ERP deficits at frontocentral electrodes (MMN: d=1.10; P3a: d=0.87; RON: d=0.77), consistent with previous studies. Each ERP component uniquely accounted for variance in amplitude and schizophrenia deficits. Amplitude reductions occurred with increasing age in both NCS and SZ patients. A small subset of patients prescribed combinations of 1st and 2nd generation antipsychotics exhibited significantly reduced MMN amplitude relative to other medication-defined subgroups. Conclusions MMN, P3a, and RON are dissociable deficits with distinct relationships to age and medication status in schizophrenia patients, potentially reflecting divergent pathophysiological processes. Reduced MMN in patients taking multiple antipsychotic medications appear to be attributable to greater severity of symptoms and functional impairments, rather than a medication effect. Significance Independent information processing deficits in schizophrenia patients may differentially contribute to the commonly observed deficits in neurocognitive and psychosocial functioning. PMID:22608970

  4. Paradoxical sleep deprivation: neurochemical, hormonal and behavioral alterations. Evidence from 30 years of research

    Directory of Open Access Journals (Sweden)

    Sergio Tufik

    2009-09-01

    Full Text Available Sleep comprises approximately one-third of a person's lifetime, but its impact on health and medical conditions remains partially unrecognized. The prevalence of sleep disorders is increasing in modern societies, with significant repercussions on people's well-being. This article reviews past and current literature on the paradoxical sleep deprivation method as well as data on its consequences to animals, ranging from behavioral changes to alterations in the gene expression. More specifically, we highlight relevant experimental studies and our group's contribution over the last three decades.O sono ocupa cerca de um terço de nossas vidas, entretanto seu impacto na saúde e sua influência nas condições patológicas ainda não foi completamente elucidado. A prevalência dos distúrbios de sono é cada vez maior, sobretudo nas regiões mais industrializadas, repercutindo diretamente no bem-estar da população. Este artigo tem como objetivo sintetizar e atualizar a literatura a respeito do método de privação de sono paradoxal e seu panorama de conseqüências desde comportamentais até genéticas em animais. Ainda, destacamos a contribuição e relevância dos estudos experimentais realizados por nosso grupo nas ultimas três décadas.

  5. Executive dysfunction among children with reading comprehension deficits.

    Science.gov (United States)

    Locascio, Gianna; Mahone, E Mark; Eason, Sarah H; Cutting, Laurie E

    2010-01-01

    Emerging research supports the contribution of executive function (EF) to reading comprehension; however, a unique pattern has not been established for children who demonstrate comprehension difficulties despite average word recognition ability (specific reading comprehension deficit; S-RCD). To identify particular EF components on which children with S-RCD struggle, a range of EF skills was compared among 86 children, ages 10 to 14, grouped by word reading and comprehension abilities: 24 average readers, 44 with word recognition deficits (WRD), and 18 S-RCD. An exploratory principal components analysis of EF tests identified three latent factors, used in subsequent group comparisons: Planning/ Spatial Working Memory, Verbal Working Memory, and Response Inhibition. The WRD group exhibited deficits (relative to controls) on Verbal Working Memory and Inhibition factors; S-RCD children performed more poorly than controls on the Planning factor. Further analyses suggested the WRD group's poor performance on EF factors was a by-product of core deficits linked to WRD (after controlling for phonological processing, this group no longer showed EF deficits). In contrast, the S-RCD group's poor performance on the planning component remained significant after controlling for phonological processing. Findings suggest reading comprehension difficulties are linked to executive dysfunction; in particular, poor strategic planning/organizing may lead to reading comprehension problems.

  6. Behavioral and neurochemical effects of chronic L-DOPA treatment on nonmotor sequelae in the hemiparkinsonian rat.

    Science.gov (United States)

    Eskow Jaunarajs, Karen L; Dupre, Kristin B; Ostock, Corinne Y; Button, Thomas; Deak, Terrence; Bishop, Christopher

    2010-10-01

    Depression and anxiety are the prevalent nonmotor symptoms that worsen quality of life for Parkinson's disease (PD) patients. Although dopamine (DA) cell loss is a commonly proposed mechanism, the reported efficacy of DA replacement therapy with L-DOPA on affective symptoms is inconsistent. To delineate the effects of DA denervation and chronic L-DOPA treatment on affective behaviors, male Sprague-Dawley rats received unilateral 6-hydroxydopamine or sham lesions and were treated daily with L-DOPA (12 mg/kg+benserazide, 15 mg/kg, subcutaneously) or vehicle (0.9% NaCl, 0.1% ascorbic acid) for 28 days before commencing investigations into anxiety (locomotor chambers, social interaction) and depression-like behaviors (forced swim test) during the OFF phase of L-DOPA. One hour after the final treatments, rats were killed and striatum, prefrontal cortex, hippocampus, and amygdala were analyzed through high-performance liquid chromatography for monoamine levels. In locomotor chambers and social interaction, DA lesions exerted mild anxiogenic effects. Surprisingly, chronic L-DOPA treatment did not improve these effects. Although DA lesion reduced climbing behaviors on day 2 of exposure to the forced swim test, chronic L-DOPA treatment did not reverse these effects. Neurochemically, L-DOPA treatment in hemiparkinsonian rats reduced norepinephrine levels in the prefrontal cortex, striatum, and hippocampus. Collectively, these data suggest that chronic L-DOPA therapy in severely DA-lesioned rats does not improve nonmotor symptoms and may impair nondopaminergic processes, indicating that long-term L-DOPA therapy does not exert necessary neuroplastic changes for improving affect.

  7. Microfluidic Platform with In-Chip Electrophoresis Coupled to Mass Spectrometry for Monitoring Neurochemical Release from Nerve Cells.

    Science.gov (United States)

    Li, Xiangtang; Hu, Hankun; Zhao, Shulin; Liu, Yi-Ming

    2016-05-17

    Chemical stimulus-induced neurotransmitter release from neuronal cells is well-documented. However, the dynamic changes in neurochemical release remain to be fully explored. In this work, a three-layered microfluidic chip was fabricated and evaluated for studying the dynamics of neurotransmitter release from PC-12 cells. The chip features integration of a nanoliter sized chamber for cell perfusion, pneumatic pressure valves for fluidic control, a microfluidic channel for electrophoretic separation, and a nanoelectrospray emitter for ionization in MS detection. Deploying this platform, a microchip electrophoresis-mass spectrometric method (MCE-MS) was developed to simultaneously quantify important neurotransmitters, including dopamine (DA), serotonin (5-HT), aspartic acid (Asp), and glutamic acid (Glu) without need for labeling or enrichment. Monitoring neurotransmitter release from PC-12 cells exposed to KCl (or alcohol) revealed that all four neurotransmitters investigated were released. Two release patterns were observed, one for the two monoamine neurotransmitters (i.e., DA and 5-HT) and another for the two amino acid neurotransmitters. Release dynamics for the two monoamine neurotransmitters was significantly different. The cells released DA most quickly and heavily in response to the stimulation. After exposure to the chemical stimulus for 4 min, the DA level in the perfusate from the cells was 86% lower than that at the beginning. Very interestingly, the cells started to release 5-HT in large quantities when they stopped releasing DA. These results suggest that DA and 5-HT are packaged into different vesicle pools and they are mobilized differently in response to chemical stimuli. The microfluidic platform proposed is proven useful for monitoring cellular release in biological studies.

  8. Effects of polychlorinated biphenyl (PCB) on regulation of thyroid-, growth-, and neurochemically related developmental processes in young rats

    Energy Technology Data Exchange (ETDEWEB)

    Juarez de Ku, L.M.

    1992-01-01

    Neonatal exposure to the toxic chemical polychlorinated biphenyl (PCB) induces hypothyroidism and retarded growth. Neonatal rats made hypothyroid by chemical or surgical means experience retarded growth and subnormal activity of choline acetyltransferase (ChAT) This study compared thyroid-, growth-, and neurochemically-related processes altered by hypothyroidism induced by other means, with PCB-induced hypothyroidism: (1) titers of thyroid stimulating hormone (TSH); (2) titers of hormones that regulate growth [growth hormone (GH), insulin-growth like factor-I (IGF-1), growth hormone releasing hormone (GHRH) and somatostatin (SS)]; or (3) brain ChAT activity. Whether PCB-induced growth retardation and other alterations are secondary to accompanying hypothyroidism rather than or in addition to a direct effect of PCB was also examined. Pregnant rats were fed chow containing 0 (controls), 62.5, 125, or 250 ppm PCB (entering offspring through placenta and milk) throughout pregnancy and lactation. Neonates exposed to PCB displayed many alterations similar to those made hypothyroid by other means: depression of overall and skeletal growth, circulating by other means: depression of overall and skeletal growth, circulating T[sub 4] levels and ChAT activity, and no change in hypothalamic GHRH and SS concentrations. Differences included a paradoxical increase in circulating GH levels, and no significant alteration of circulation IGF-1 and TSH levels and pituitary GH and TSH levels (although trends were in the expected direction). Thus, PCB-induced hypothyroidism may partially cause altered skeletal growth, circulating GH and TSH concentrations, and ChAT activity. Both T[sub 4] and T[sub 3] injections returned circulating TSH and GH levels and pituitary TSH content toward control levels; T[sub 3] restored skeletal, but not overall growth; and T[sub 4] elevated ChAT activity.

  9. An allosteric enhancer of M4 muscarinic acetylcholine receptor function inhibits behavioral and neurochemical effects of cocaine

    Science.gov (United States)

    Dencker, Ditte; Weikop, Pia; Sørensen, Gunnar; Woldbye, David P. D.; Wörtwein, Gitta; Wess, Jürgen; Fink-Jensen, Anders

    2014-01-01

    Rationale The mesostriatal dopamine system plays a key role in mediating the reinforcing effects of psychostimulant drugs like cocaine. The muscarinic M4 acetylcholine receptor subtype is centrally involved in regulation of dopamine release in striatal areas. Consequently, striatal M4 receptors could be a novel target for modulating psychostimulant effects of cocaine. Objectives For the first time, we here addressed this issue by investigating the effects of a novel selective positive allosteric modulator of M4 receptors, VU0152100, on cocaine-induced behavioral and neurochemical effects in mice. Methods To investigate the effect of VU0152100 on the acute reinforcing effects of cocaine, we use an acute-cocaine self-administration model. We used in vivo microdialysis to investigate whether the effects of VU0152100 in the behavioral studies were mediated via effects on dopaminergic neurotransmission. In addition the effect of VU0152100 on cocaine-induced hyperactivity and rotarod performance was evaluated. Results We found that VU0152100 caused a prominent reduction in cocaine self-administration, cocaine-induced hyperlocomotion, and cocaine-induced striatal dopamine increase, without affecting motor performance. Consistent with these effects of VU0152100 being mediated via M4 receptors, its inhibitory effects on cocaine-induced increases in striatal dopamine were abolished in M4 receptor knockout mice. Furthermore, selective deletion of the M4 receptor gene in dopamine D1 receptor-expressing neurons resulted in a partial reduction of the VU0152100 effect, indicating that VU0152100 partly regulates dopaminergic neurotransmission via M4 receptors co-localized with D1 receptors. Conclusions These results show that positive allosteric modulators of the M4 receptor deserve attention as agents in the future treatment of cocaine abuse. PMID:22648127

  10. Neurochemical and Neuroanatomical Plasticity Following Memory Training and Yoga Interventions in Older Adults with Mild Cognitive Impairment

    Directory of Open Access Journals (Sweden)

    Hongyu Yang

    2016-11-01

    Full Text Available Behavioral interventions are becoming increasingly popular approaches to ameliorate age-related cognitive decline, but their underlying neurobiological mechanisms and clinical efficiency have not been fully elucidated. The present study explored brain plasticity associated with two behavioral interventions, memory enhancement training (MET and a mind-body practice (yogic meditation, in healthy seniors with mild cognitive impairment (MCI using structural magnetic resonance imaging (MRI and proton magnetic resonance spectroscopy (1H-MRS. Senior participants (age ≥ 55 years with MCI were randomized to the MET or yogic meditation interventions. For both interventions, participants completed either MET training or Kundalini yoga for 60-min sessions over 12 weeks, with 12-min daily homework assignments. Gray matter volume and metabolite concentrations in the dorsal anterior cingulate cortex (dACC and bilateral hippocampus were measured by structural MRI and 1H-MRS at baseline and after 12 weeks of training. Metabolites measured included glutamate-glutamine (Glx, choline-containing compounds (Cho, including glycerophosphocholine and phosphocholine, gamma-aminobutyric acid (GABA, and N-acetyl aspartate and N-acetylaspartyl-glutamate (NAA-NAAG. In total, 11 participants completed MET and 14 completed yogic meditation for this study. Structural MRI analysis showed an interaction between time and group in dACC, indicating a trend towards increased gray matter volume after the MET intervention. 1H-MRS analysis showed an interaction between time and group in choline-containing compounds in bilateral hippocampus, induced by significant decreases after the MET intervention. Though preliminary, our results suggest that memory training induces structural and neurochemical plasticity in seniors with mild cognitive impairment. Further research is needed to determine whether mind-body interventions like yoga yield similar neuroplastic changes.

  11. Aripiprazole Selectively Reduces Motor Tics in a Young Animal Model for Tourette’s Syndrome and Comorbid Attention Deficit and Hyperactivity Disorder

    Directory of Open Access Journals (Sweden)

    Francesca Rizzo

    2018-02-01

    Full Text Available Tourette’s syndrome (TS is a neurodevelopmental disorder characterized primarily by motor and vocal tics. Comorbidities such as attention deficit and hyperactivity disorder (ADHD are observed in over 50% of TS patients. We applied aripiprazole in a juvenile rat model that displays motor tics and hyperactivity. We additionally assessed the amount of ultrasonic vocalizations (USVs as an indicator for the presence of vocal tics and evaluated the changes in the striatal neurometabolism using in vivo proton magnetic resonance spectroscopy (1H-MRS at 11.7T. Thirty-one juvenile spontaneously hypertensive rats (SHRs underwent bicuculline striatal microinjection and treatment with either aripiprazole or vehicle. Control groups were sham operated and sham injected. Behavior, USVs, and striatal neurochemical profile were analyzed at early, middle, and late adolescence (postnatal days 35 to 50. Bicuculline microinjections in the dorsolateral striatum induced motor tics in SHR juvenile rats. Acute aripiprazole administration selectively reduced both tic frequency and latency, whereas stereotypies, USVs, and hyperactivity remained unaltered. The striatal neurochemical profile was only moderately altered after tic-induction and was not affected by systemic drug treatment. When applied to a young rat model that provides high degrees of construct, face, and predictive validity for TS and comorbid ADHD, aripiprazole selectively reduces motor tics, revealing that tics and stereotypies are distinct phenomena in line with clinical treatment of patients. Finally, our 1H-MRS results suggest a critical revision of the striatal role in the hypothesized cortico-striatal dysregulation in TS pathophysiology.

  12. Attention Deficit Hyperactivity Disorder (ADHD)

    Centers for Disease Control (CDC) Podcasts

    2014-04-10

    This podcast discusses Attention Deficit Hyperactivity Disorder, or ADHD, the most common behavioral disorder in children. Learn about symptoms, risk factors, and treatment.  Created: 4/10/2014 by National Center on Birth Defects and Developmental Disabilities (NCBDDD).   Date Released: 5/7/2014.

  13. Persistent Motor Deficits in DAMP

    OpenAIRE

    J Gordon Millichap

    2000-01-01

    Motor control in ability to perform everyday and spare-time activities was assessed at 11 to 12 years of age in 10 boys with deficits in attention, motor control and perception (DAMP) and compared with a group of 20 boys without DAMP.

  14. Attention Deficit and EEG Analysis

    OpenAIRE

    J Gordon Millichap

    1992-01-01

    Computerized power spectral analysis (PSA), permitting topographic representation and statistical analysis of EEG, of 25 right-handed males, 9-12 years of age with attention deficit hyperactivity disorder was used in studies from the Departments of Psychology, Pediatrics (Neurology) and Computing Center, University of Tennessee and East Tennessee Children’s Hospital, Knoxville, TN.

  15. Proprioceptive deficits after ACL injury

    NARCIS (Netherlands)

    E. Otten; K. Postema; S.M. Lephart; M.P. Arnold; P.U. Dijkstra; A. Gokeler; L. Engebretsen; E. Ageberg; T.E. Hewett; Anne Benjaminse; Engelhardt M

    2012-01-01

    OBJECTIVE: To establish the clinical relevance of proprioceptive deficits reported after anterior cruciate ligament (ACL) injury. MATERIAL AND METHODS: A literature search was done in electronic databases from January 1990 to June 2009. Inclusion criteria for studies were ACL deficient (ACL-D) and

  16. Acquired prosopagnosia without word recognition deficits.

    Science.gov (United States)

    Susilo, Tirta; Wright, Victoria; Tree, Jeremy J; Duchaine, Bradley

    2015-01-01

    It has long been suggested that face recognition relies on specialized mechanisms that are not involved in visual recognition of other object categories, including those that require expert, fine-grained discrimination at the exemplar level such as written words. But according to the recently proposed many-to-many theory of object recognition (MTMT), visual recognition of faces and words are carried out by common mechanisms [Behrmann, M., & Plaut, D. C. ( 2013 ). Distributed circuits, not circumscribed centers, mediate visual recognition. Trends in Cognitive Sciences, 17, 210-219]. MTMT acknowledges that face and word recognition are lateralized, but posits that the mechanisms that predominantly carry out face recognition still contribute to word recognition and vice versa. MTMT makes a key prediction, namely that acquired prosopagnosics should exhibit some measure of word recognition deficits. We tested this prediction by assessing written word recognition in five acquired prosopagnosic patients. Four patients had lesions limited to the right hemisphere while one had bilateral lesions with more pronounced lesions in the right hemisphere. The patients completed a total of seven word recognition tasks: two lexical decision tasks and five reading aloud tasks totalling more than 1200 trials. The performances of the four older patients (3 female, age range 50-64 years) were compared to those of 12 older controls (8 female, age range 56-66 years), while the performances of the younger prosopagnosic (male, 31 years) were compared to those of 14 younger controls (9 female, age range 20-33 years). We analysed all results at the single-patient level using Crawford's t-test. Across seven tasks, four prosopagnosics performed as quickly and accurately as controls. Our results demonstrate that acquired prosopagnosia can exist without word recognition deficits. These findings are inconsistent with a key prediction of MTMT. They instead support the hypothesis that face

  17. Comprehensive characterization of neurochemicals in three zebrafish chemical models of human acute organophosphorus poisoning using liquid chromatography-tandem mass spectrometry.

    Science.gov (United States)

    Gómez-Canela, Cristian; Tornero-Cañadas, Daniel; Prats, Eva; Piña, Benjamí; Tauler, Romà; Raldúa, Demetrio

    2018-02-01

    There is a growing interest in biological models to investigate the effect of neurotransmitter dysregulation on the structure and function of the central nervous system (CNS) at different stages of development. Zebrafish, a vertebrate model increasingly used in neurobiology and neurotoxicology, shares the common neurotransmitter systems with mammals, including glutamate, GABA, glycine, dopamine, norepinephrine, epinephrine, serotonin, acetylcholine, and histamine. In this study, we have evaluated the performance of liquid chromatography-tandem mass spectrometry (LC-MS/MS) for the multiresidue determination of neurotransmitters and related metabolites. In a first step, ionization conditions were tested in positive electrospray mode and optimum fragmentation patterns were determined to optimize two selected reaction monitoring (SRM) transitions. Chromatographic conditions were optimized considering the chemical structure and chromatographic behavior of the analyzed compounds. The best performance was obtained with a Synergy Polar-RP column, which allowed the separation of the 38 compounds in 30 min. In addition, the performance of LC-MS/MS was studied in terms of linearity, sensitivity, intra- and inter-day precision, and overall robustness. The developed analytical method was able to quantify 27 of these neurochemicals in zebrafish chemical models for mild (P1), moderate (P2), and severe (P3) acute organophosphorus poisoning (OPP). The results show a general depression of synaptic-related neurochemicals, including the excitatory and inhibitory amino acids, as well as altered phospholipid metabolism, with specific neurochemical profiles associated to the different grades of severity. These results confirmed that the developed analytical method is a new tool for neurotoxicology research using the zebrafish model.

  18. Neurochemical differences in learning and memory paradigms among rats supplemented with anthocyanin-rich blueberry diets and exposed to acute doses of 56Fe particles

    Science.gov (United States)

    Poulose, Shibu M.; Rabin, Bernard M.; Bielinski, Donna F.; Kelly, Megan E.; Miller, Marshall G.; Thanthaeng, Nopporn; Shukitt-Hale, Barbara

    2017-02-01

    The protective effects of anthocyanin-rich blueberries (BB) on brain health are well documented and are particularly important under conditions of high oxidative stress, which can lead to "accelerated aging." One such scenario is exposure to space radiation, consisting of high-energy and -charge particles (HZE), which are known to cause cognitive dysfunction and deleterious neurochemical alterations. We recently tested the behavioral and neurochemical effects of acute exposure to HZE particles such as 56Fe, within 24-48 h after exposure, and found that radiation primarily affects memory and not learning. Importantly, we observed that specific brain regions failed to upregulate antioxidant and anti-inflammatory mechanisms in response to this insult. To further examine these endogenous response mechanisms, we have supplemented young rats with diets rich in BB, which are known to contain high amounts of antioxidant-phytochemicals, prior to irradiation. Exposure to 56Fe caused significant neurochemical changes in hippocampus and frontal cortex, the two critical regions of the brain involved in cognitive function. BB supplementation significantly attenuated protein carbonylation, which was significantly increased by exposure to 56Fe in the hippocampus and frontal cortex. Moreover, BB supplementation significantly reduced radiation-induced elevations in NADPH-oxidoreductase-2 (NOX2) and cyclooxygenase-2 (COX-2), and upregulated nuclear factor erythroid 2-related factor 2 (Nrf2) in the hippocampus and frontal cortex. Overall results indicate that 56Fe particles may induce their toxic effects on hippocampus and frontal cortex by reactive oxygen species (ROS) overload, which can cause alterations in the neuronal environment, eventually leading to hippocampal neuronal death and subsequent impairment of cognitive function. Blueberry supplementation provides an effective preventative measure to reduce the ROS load on the CNS in an event of acute HZE exposure.

  19. Cognitive deficits in obstructive sleep apnea: Insights from a meta-review and comparison with deficits observed in COPD, insomnia, and sleep deprivation.

    Science.gov (United States)

    Olaithe, Michelle; Bucks, Romola S; Hillman, David R; Eastwood, Peter R

    2017-03-30

    Obstructive sleep apnea (OSA) is a nocturnal breathing disorder that is associated with cognitive impairment. The primary determinants of cognitive deficits in OSA are thought to be sleep disruption and blood gas abnormalities. Cognitive impairment is also seen in other disorders that are characterised primarily by sleep disturbance (e.g., sleep restriction/deprivation, insomnia) or hypoxia/hypercarbia (e.g., chronic obstructive pulmonary disease (COPD)). Assessment of the cognitive deficits observed in these other disorders could help better define the mechanisms underlying cognitive deficits in OSA. This study utilised meta-review methodology to examine the findings from systematic reviews and meta-analyses of the effects of untreated OSA, COPD, insomnia, and sleep deprivation on cognitive function in adults, compared with norms or controls. Eighteen papers met inclusion criteria: seven in OSA, two in insomnia, five in COPD, and four in sleep deprivation. OSA and COPD were both accompanied by deficits in attention, memory, executive function, psychomotor function, and language abilities, suggesting that hypoxia/hypercarbia may be an important determinant of deficits in these domains in OSA. Both OSA and sleep deprivation studies were accompanied by deficits in attention and memory, suggesting that short-term sleep disturbance in OSA may contribute to deficits in these domains. Visuospatial deficits were unique to OSA, suggesting the contribution of a mechanism other than sleep disturbance and hypoxia/hypercarbia to this problem. Our findings suggest that the cognitive deficits associated with untreated OSA are multidimensional, with different physiological disturbances responsible for differing cognitive problems. Copyright © 2017 Elsevier Ltd. All rights reserved.

  20. Pragmatic Communication Deficits in Children with Epilepsy

    Science.gov (United States)

    Broeders, Mark; Geurts, Hilde; Jennekens-Schinkel, Aag

    2010-01-01

    Background: Various psychiatric and neurological disorders including epilepsy have been associated with language deficits. Pragmatic language deficits, however, have seldom been the focus of earlier studies in children with epilepsy. Moreover, it is unknown whether these pragmatic deficits are related to general intellectual functioning. Both…

  1. Neural oscillatory deficits in schizophrenia predict behavioral and neurocognitive impairments

    Directory of Open Access Journals (Sweden)

    Antigona eMartinez

    2015-07-01

    Full Text Available Paying attention to visual stimuli is typically accompanied by event-related desynchronizations (ERD of ongoing alpha (7-14 Hz activity in visual cortex. The present study used time-frequency based analyses to investigate the role of impaired alpha ERD in visual processing deficits in schizophrenia (Sz. Subjects viewed sinusoidal gratings of high (HSF and low (LSF spatial frequency designed to test functioning of the parvo- versus magnocellular pathways, respectively. Patients with Sz and healthy controls paid attention selectively to either the LSF or HSF gratings which were presented in random order. Event-related brain potentials (ERPs were recorded to all stimuli. As in our previous study, it was found that Sz patients were selectively impaired at detecting LSF target stimuli and that ERP amplitudes to LSF stimuli were diminished, both for the early sensory-evoked components and for the attend minus unattend difference component (the Selection Negativity, which is generally regarded as a specific index of feature-selective attention. In the time-frequency domain, the differential ERP deficits to LSF stimuli were echoed in a virtually absent theta-band phase locked response to both unattended and attended LSF stimuli (along with relatively intact theta-band activity for HSF stimuli. In contrast to the theta-band evoked responses which were tightly stimulus locked, stimulus-induced desynchronizations of ongoing alpha activity were not tightly stimulus locked and were apparent only in induced power analyses. Sz patients were significantly impaired in the attention-related modulation of ongoing alpha activity for both HSF and LSF stimuli. These deficits correlated with patients’ behavioral deficits in visual information processing as well as with visually based neurocognitive deficits. These findings suggest an additional, pathway-independent, mechanism by which deficits in early visual processing contribute to overall cognitive impairment in

  2. Neurochemical Changes in the Mouse Hippocampus Underlying the Antidepressant Effect of Genetic Deletion of P2X7 Receptors.

    Directory of Open Access Journals (Sweden)

    Cecilia Csölle

    Full Text Available Recent investigations have revealed that the genetic deletion of P2X7 receptors (P2rx7 results in an antidepressant phenotype in mice. However, the link between the deficiency of P2rx7 and changes in behavior has not yet been explored. In the present study, we studied the effect of genetic deletion of P2rx7 on neurochemical changes in the hippocampus that might underlie the antidepressant phenotype. P2X7 receptor deficient mice (P2rx7-/- displayed decreased immobility in the tail suspension test (TST and an attenuated anhedonia response in the sucrose preference test (SPT following bacterial endotoxin (LPS challenge. The attenuated anhedonia was reproduced through systemic treatments with P2rx7 antagonists. The activation of P2rx7 resulted in the concentration-dependent release of [(3H]glutamate in P2rx7+/+ but not P2rx7-/- mice, and the NR2B subunit mRNA and protein was upregulated in the hippocampus of P2rx7-/- mice. The brain-derived neurotrophic factor (BDNF expression was higher in saline but not LPS-treated P2rx7-/- mice; the P2rx7 antagonist Brilliant blue G elevated and the P2rx7 agonist benzoylbenzoyl ATP (BzATP reduced BDNF level. This effect was dependent on the activation of NMDA and non-NMDA receptors but not on Group I metabotropic glutamate receptors (mGluR1,5. An increased 5-bromo-2-deoxyuridine (BrdU incorporation was also observed in the dentate gyrus derived from P2rx7-/- mice. Basal level of 5-HT was increased, whereas the 5HIAA/5-HT ratio was lower in the hippocampus of P2rx7-/- mice, which accompanied the increased uptake of [(3H]5-HT and an elevated number of [(3H]citalopram binding sites. The LPS-induced elevation of 5-HT level was absent in P2rx7-/- mice. In conclusion there are several potential mechanisms for the antidepressant phenotype of P2rx7-/- mice, such as the absence of P2rx7-mediated glutamate release, elevated basal BDNF production, enhanced neurogenesis and increased 5-HT bioavailability in the hippocampus.

  3. Jugular venous overflow of noradrenaline from the brain: a neurochemical indicator of cerebrovascular sympathetic nerve activity in humans

    Science.gov (United States)

    Mitchell, David A; Lambert, Gavin; Secher, Niels H; Raven, Peter B; van Lieshout, Johannes; Esler, Murray D

    2009-01-01

    A novel neurochemical method was applied for studying the activity of sympathetic nerves in the human cerebral vascular system. The aim was to investigate whether noradrenaline plasma kinetic measurements made with internal jugular venous sampling reflect cerebrovascular sympathetic activity. A database was assembled of fifty-six healthy subjects in whom total body noradrenaline spillover (indicative of whole body sympathetic nervous activity), brain noradrenaline spillover and brain lipophlic noradrenaline metabolite (3,4-dihydroxyphenolglycol (DHPG) and 3-methoxy-4-hydroxyphenylglycol (MHPG)) overflow rates were measured. These measurements were also made following ganglion blockade (trimethaphan, n= 6), central sympathetic inhibition (clonidine, n= 4) and neuronal noradrenaline uptake blockade (desipramine, n= 13) and in a group of patients (n= 9) with pure autonomic failure (PAF). The mean brain noradrenline spillover and brain noradrenaline metabolite overflow in healthy subjects were 12.5 ± 1.8, and 186.4 ± 25 ng min−1, respectively, with unilateral jugular venous sampling for both. Total body noradrenaline spillover was 605.8 ng min−1± 34.4 ng min−1. As expected, trimethaphan infusion lowered brain noradrenaline spillover (P= 0.03), but perhaps surprisingly increased jugular overflow of brain metabolites (P= 0.01). Suppression of sympathetic nervous outflow with clonidine lowered brain noradrenaline spillover (P= 0.004), without changing brain metabolite overflow (P= 0.3). Neuronal noradrenaline uptake block with desipramine lowered the transcranial plasma extraction of tritiated noradrenaline (P= 0.001). The PAF patients had 77% lower brain noradrenaline spillover than healthy recruits (P= 0.06), indicating that in them sympathetic nerve degeneration extended to the cerebral circulation, but metabolites overflow was similar to healthy subjects (P= 0.3). The invariable discordance between noradrenline spillover and noradrenaline metabolite overflow

  4. Wireless Instantaneous Neurotransmitter Concentration System-based amperometric detection of dopamine, adenosine, and glutamate for intraoperative neurochemical monitoring.

    Science.gov (United States)

    Agnesi, Filippo; Tye, Susannah J; Bledsoe, Jonathan M; Griessenauer, Christoph J; Kimble, Christopher J; Sieck, Gary C; Bennet, Kevin E; Garris, Paul A; Blaha, Charles D; Lee, Kendall H

    2009-10-01

    WINCS, which is designed in compliance with FDA-recognized consensus standards for medical electrical device safety, successfully measured dopamine, glutamate, and adenosine, both in vitro and in vivo. The WINCS detected striatal dopamine release at the implanted CFM during DBS of the MFB. The DBS-evoked adenosine release in the rat thalamus and MCS-evoked glutamate release in the pig cortex were also successfully measured. Overall, in vitro and in vivo testing demonstrated signals comparable to a commercial hardwired electrochemical system for FPA. By incorporating FPA, the chemical repertoire of WINCS-measurable neurotransmitters is expanded to include glutamate and other nonelectroactive species for which the evolving field of enzyme-linked biosensors exists. Because many neurotransmitters are not electrochemically active, FPA in combination with enzyme-linked microelectrodes represents a powerful intraoperative tool for rapid and selective neurochemical sampling in important anatomical targets during functional neurosurgery.

  5. The efficacy of neurofeedback in the management of children with attention deficit/hyperactivity disorder.

    Science.gov (United States)

    Baydala, L; Wikman, E

    2001-09-01

    Attention deficit/hyperactivity disorder (ADHD) is a behavioural disorder characterized by an inappropriate level of inattention with or without impulsivity or overactivity. The estimated prevalence of ADHD is 7% to 10% in boys and 3% in girls aged four to 11 years. The higher prevalence in boys is believed to be the result of a referral bias because boys with ADHD are more disruptive and aggressive, and, therefore, more likely to be referred to specialty clinics. ADHD is caused by a combination of biological - often genetically determined neurochemical disturbances - and environmental disadvantages that are associated with learning difficulties, behavioural problems and social rejection. The identification and treatment of children with ADHD are essential in preventing or at least minimizing the serious complications associated with this disorder. Stimulant medications are the most effective means of symptomatic control of ADHD symptoms, and the safety and efficacy of these medications is well established in the literature. Despite the known efficacy of stimulant medications, alternatives are often sought by parents of children with ADHD. A number of alternative and controversial treatments for ADHD are available, including dietary management, nutritional supplementation, vision therapy, hypnotherapy, guided imagery, relaxation training and electroencephalogram (EEG) neurofeedback. Published well controlled scientific studies either to support or refute the effectiveness of EEG neurofeedback for children with ADHD are not available. At the present time, EEG neurofeedback needs to be considered as an experimental treatment, the validity of which has not yet been determined.

  6. The Emerging Neurobiology of Attention Deficit Hyperactivity Disorder: The Key Role of the Prefrontal Association Cortex

    Science.gov (United States)

    Arnsten, Amy F.T.

    2009-01-01

    Attention deficit/hyperactivity disorder (ADHD) is characterized by symptoms of inattention, impulsivity, and locomotor hyperactivity. Recent advances in neurobiology, imaging, and genetics have led to a greater understanding of the etiology and treatment of ADHD. Studies have found that ADHD is associated with weaker function and structure of prefrontal cortex (PFC) circuits, especially in the right hemisphere. The prefrontal association cortex plays a crucial role in regulating attention, behavior, and emotion, with the right hemisphere specialized for behavioral inhibition. The PFC is highly dependent on the correct neurochemical environment for proper function: noradrenergic stimulation of postsynaptic alpha-2A adrenoceptors and dopaminergic stimulation of D1 receptors is necessary for optimal prefrontal function. ADHD is associated with genetic changes that weaken catecholamine signaling and, in some patients, with slowed PFC maturation. Effective pharmacologic treatments for ADHD all enhance catecholamine signaling in the PFC and strengthen its regulation of attention and behavior. Recent animal studies show that therapeutic doses of stimulant medications preferentially increase norepinephrine and, to a lesser extent, dopamine, in the PFC. These doses reduce locomotor activity and improve PFC regulation of attention and behavior through enhanced catecholamine stimulation of alpha-2A and D1 receptors. These findings in animals are consistent with improved PFC function in normal human subjects and, more prominently, in patients with ADHD. Thus, a highly cohesive story is emerging regarding the etiology and treatment of ADHD. PMID:20596295

  7. Visuospatial deficits of dyslexic children.

    Science.gov (United States)

    Lipowska, Malgorzata; Czaplewska, Ewa; Wysocka, Anna

    2011-04-01

    The visuospatial deficit is recognized as typical for dyslexia only in some definitions. However problems with visuospatial orientation may manifest themselves as difficulties with letter identification or the memorizing and recalling of sign sequences, something frequently experienced by dyslexics. The experimental group consisted of 62 children with developmental dyslexia. The control group consisted of 67 pupils with no diagnosed deficits, matched to the clinical group in terms of age. We used the Clock Drawing Test (CDT), the Spatial Span subtest from the Wechsler Memory Scale - third edition (WMS - III), the Rey-Osterrieth Complex Figure Test in order to analyze visuospatial functioning. The results show that dyslexics experienced problems with visuospatial functioning, however only while performing difficult tasks. Significant group differences were found for the Clock Drawing Test, Spatial Span - Backward and the precision of figure coping in the Rey-Osterrieth Test. In addition, the results of dyslexic boys were lower than those obtained by all other groups. Our findings provide support for the hypothesis concerning visual deficit as characteristic for dyslexia.

  8. Species, sex and individual differences in the vasotocin/vasopressin system: relationship to neurochemical signaling in the social behavior neural network.

    Science.gov (United States)

    Albers, H Elliott

    2015-01-01

    Arginine-vasotocin (AVT)/arginine vasopressin (AVP) are members of the AVP/oxytocin (OT) superfamily of peptides that are involved in the regulation of social behavior, social cognition and emotion. Comparative studies have revealed that AVT/AVP and their receptors are found throughout the "social behavior neural network (SBNN)" and display the properties expected from a signaling system that controls social behavior (i.e., species, sex and individual differences and modulation by gonadal hormones and social factors). Neurochemical signaling within the SBNN likely involves a complex combination of synaptic mechanisms that co-release multiple chemical signals (e.g., classical neurotransmitters and AVT/AVP as well as other peptides) and non-synaptic mechanisms (i.e., volume transmission). Crosstalk between AVP/OT peptides and receptors within the SBNN is likely. A better understanding of the functional properties of neurochemical signaling in the SBNN will allow for a more refined examination of the relationships between this peptide system and species, sex and individual differences in sociality. Copyright © 2014 Elsevier Inc. All rights reserved.

  9. Anti-depressant like effect of curcumin and its combination with piperine in unpredictable chronic stress-induced behavioral, biochemical and neurochemical changes.

    Science.gov (United States)

    Bhutani, Mohit Kumar; Bishnoi, Mahendra; Kulkarni, Shrinivas K

    2009-03-01

    Curcumin, a yellow pigment extracted from rhizomes of the plant Curcuma longa (turmeric), has been widely used as food additive and also as a herbal medicine throughout Asia. The present study was designed to study the pharmacological, biochemical and neurochemical effects of daily administration of curcumin to rats subjected to chronic unpredictable stress. Curcumin treatment (20 and 40 mg/kg, i.p., 21 days) significantly reversed the chronic unpredictable stress-induced behavioral (increase immobility period), biochemical (increase monoamine oxidase activity) and neurochemical (depletion of brain monoamine levels) alterations. The combination of piperine (2.5 mg/kg, i.p., 21 days), a bioavailability enhancer, with curcumin (20 and 40 mg/kg, i.p., 21 days) showed significant potentiation of its anti-immobility, neurotransmitter enhancing (serotonin and dopamine) and monoamine oxidase inhibitory (MAO-A) effects as compared to curcumin effect per se. This study provided a scientific rationale for the use of curcumin and its co-administration with piperine in the treatment of depressive disorders.

  10. Association between the attention deficits and delinquency

    Directory of Open Access Journals (Sweden)

    Robert Opora

    2011-12-01

    Full Text Available In the society we can find a lot of prejudices concerning AD/HD. The article contains facts and evidence based on research presenting that the delinquency is very often a distant complication of attention deficits but it doesn’t mean that a child with attention deficits has to be delinquent. The article describes the association between the attention deficits and delinquency. There are presented some risk factors coming from the attention deficits and protective factors which let the child follow the social norms. The research was based on 108 delinquent juveniles staying under the probation supervision. The purpose of the research was to evaluate the frequency of the attention deficits among delinquent juveniles staying under supervision. The research findings concern also the association between the attention deficit and external behavioural disorders. In the summary several conditions are described which are important to protect children with attention deficit from delinquency.

  11. [Reading comprehension of students with attention deficit hyperactivity disorder: what is the role of executive functions?].

    Science.gov (United States)

    Miranda-Casas, A; Fernández, M I; Robledo, P; García-Castellar, R

    2010-03-03

    Deficits in reading comprehension of children with attention deficit hyperactivity disorder (ADHD) have received scarce attention. However, to establish the underlying cognitive processes of ADHD and deficits in reading comprehension association could be essential for deeply understanding neurobiological bases of reading comprehension. To examine the contribution of verbal fluency, reading fluency, and executive functions (working memory, attention and suppression mechanism) in predicting mental processes of texts comprehension. The participants in the study were 42 students, 12 to 16 year old, with a clinical diagnosis of ADHD. A battery of tests was administered to measure cognitive processes and reading processes. Stepwise regression analysis carried out showed that the score in verbal fluency was the best single predictor of reading comprehension. Furthermore executive functions, but not reading fluency, made a significant contribution to reading comprehension. These findings underline the need for consideration of the role of executive functions in assessment and treatment of reading comprehension deficits of students with ADHD.

  12. Non-literal language deficits in mild cognitive impairment.

    Science.gov (United States)

    Cardoso, Sandra; Silva, Dina; Maroco, João; de Mendonça, Alexandre; Guerreiro, Manuela

    2014-12-01

    Verbal language deteriorates in Alzheimer's disease, contributing to dramatic disturbances in the ability to communicate. The presence of language disturbances may be detected at earlier phases of the neurodegenerative process, like mild cognitive impairment (MCI). In daily verbal interactions, people mostly use literal language, but sometimes they employ non-literal language, which requires listeners to interpret messages beyond the plain meaning of the words and can be quite demanding. In the present study, we tested the hypotheses that patients with MCI may have deficits in non-literal language, and these deficits are more pronounced than deficits in literal language. Participants were recruited in a private memory clinic and senior universities. General cognitive evaluation included a comprehensive neuropsychological battery, the Mini-Mental State Examination, and the instrumental activities of daily living scale. Literal language was assessed with the semantic decision test, Token Test, and literal text comprehension test, and non-literal language with the proverbs comprehension, idiomatic expressions and non-literal text comprehension tests. Fifty-two participants with MCI and 31 controls were recruited. Patients with MCI had lower scores in all complex language tests, both literal (Token Test, semantic decision and literal text) and non-literal (proverbs, idiomatic expressions, and non-literal text), than the controls; the difference in literal text score was marginally significant. As much as 69% of MCI participants had deficits (performance below 1.5 SD of the mean) on at least one of the complex language tasks. Deficits were more frequent on the proverbs comprehension and semantic decision tests, and the deficits on these tests did not significantly differ from that on the Token Test. Patients with MCI are hindered in understanding complex language, both literal and non-literal. In daily living, these complex language deficits could compromise effective

  13. Offsetting deficit conceptualisations: methodological considerations for higher education research

    Directory of Open Access Journals (Sweden)

    Lynn Coleman

    2016-06-01

    Full Text Available This paper contributes to the current introspection in the academic development community that critiques the persistent conceptualisations of students as deficient. Deficit discourses are also implicated in many of the student support, curriculum and pedagogic initiatives employed across the higher education sector. The argument developed here, unlike most of the existing debates which focus on pedagogic or institutional initiatives, explores how the research interests and methodological choices of academic developers and researchers could incorporate sensitivity against deficit conceptions and foster more contextualised accounts of students and their learning. This article uses an ethnographic study into the assignment practices of vocational higher education students to show how certain methodological and theoretical choices engender anti-deficit conceptualisations. The study’s analytic framework uses the concepts of literacy practices and knowledge recontextualisation to place analytic attention on both the students’ assignment practices and the influence of curriculum decision making on such practices. The significance of this dual focus is its ability to capture the complexity of students’ meaning-making during assignment production, without remaining silent about the structuring influence of the curriculum. I argue in this paper that the focus on both students and curriculum is able to offer contextualised accounts of students’ interpretations and enacted experiences of their assessment and curriculum environment. Exploring the multidimensional nature of student learning experiences in ways that accommodate the influence of various contextual realities brings researchers and their research agendas closer to offsetting deficit conceptualisation.

  14. Stigma in attention deficit hyperactivity disorder.

    Science.gov (United States)

    Mueller, Anna K; Fuermaier, Anselm B M; Koerts, Janneke; Tucha, Lara

    2012-09-01

    Attention deficit hyperactivity disorder (ADHD) is a frequently diagnosed disorder in child- and adulthood with a high impact affecting multiple facets of social life. Therefore, patients suffering from ADHD are at high risk to be confronted with stigma, prejudices, and discrimination. A review of the empirical research in the field of ADHD with regard to stigma was performed. The findings of investigations in this field were clustered in different categories, including stigma in children with ADHD, stigma in adults with ADHD, stigma in relatives or in people close to a patient with ADHD, and the influence of stigma on authorities' attitudes toward patients with ADHD. Variables identified to contribute to stigma in ADHD are public's uncertainty concerning the reliability/validity of an ADHD diagnosis and the related diagnostic assessment, public's perceived dangerousness of individuals with ADHD, socio-demographical factors as age, gender, and ethnicity of the respondent or the target individual with ADHD, stigmatization of ADHD treatment, for example public's skepticism toward ADHD medication and disclosure of diagnostic status as well as medication status of the individual with ADHD. The contribution of stigma associated with ADHD can be conceptualized as an underestimated risk factor, affecting treatment adherence, treatment efficacy, symptom aggravation, life satisfaction, and mentally well-being of individuals affected by ADHD. Public as well as health professionals' concepts about ADHD are highly diverse, setting individuals with an ADHD diagnosis at greater risk to get stigmatized.

  15. Two deficits and economic growth: Case of CEE countries in transition

    OpenAIRE

    Gurgul, Henryk; Lach, Łukasz

    2012-01-01

    The main goal of this contribution was to provide evidence on the dynamic interdependencies between economic growth and budget and trade deficits in ten new EU members in transition in the last decade. It is worth to note that beside establishing directions of causal relationships this paper also derived some suggestions on signs of the dynamic dependencies analyzed. The outcomes of this paper confirmed that the budget deficits were significantly slowing down the GDP growth rates in case...

  16. Prenatal smoking predicts non-response to an intervention targeting attention - deficit/hyperactivity problems in elementary schoolchildren

    NARCIS (Netherlands)

    Vuijk, P.J.; van Lier, P.A.C.; Huizink, A.C.; Verhulst, F.C.; Crijnen, A.A.M.

    2006-01-01

    Background: Some evidence suggests that prenatal exposure to maternal smoking contributes to the etiology of Attention-Deficit/Hyperactivity Disorder (ADHD). The present study tested an intervention targeting disruptive behavior to establish whether exposure to maternal smoking during pregnancy

  17. Contributions lexicographiques

    Directory of Open Access Journals (Sweden)

    France Bezlaj

    1955-12-01

    Full Text Available Dans les »Novice« du 6 avril 1859, p. 108, Fr. Pohorski (probablement un pseudonyme d'un auteur inconnu publia des matériaux lexicographiques sous le title »Quelques mots rares de Pohorje en Styrie«. Cette contribution passa inaperçue et Pleteršnik ne cite dans son dictionnaire que quelques-uns de ces mots qu'il a tirés d'une autre source. Dans un passé plus récent, J. Kelemina prit dans ce recueil le nom commun tega, teha »chalet de montagne«, die Taie en all. Carinth (Slovenski etnograf VI-VIII 323  *tegia, (prérom. Attegia (Meyer-Lübke, REW 761 et sot »chemin de montagne« (SR VIII 88, ce qui pourrait venir, après avoir passé par le roman, de (prérom.

  18. Metallic Burden of Deciduous Teeth and Childhood Behavioral Deficits

    Directory of Open Access Journals (Sweden)

    Tony J.H. Chan

    2015-06-01

    Full Text Available Attention Deficit/Hyperactivity Disorder (ADHD affects 5%–8% of children in the U.S. (10% of males and 4% of females. The contributions of multiple metal exposures to the childhood behavioral deficits are unclear, although particular metals have been implicated through their neurotoxicity. The objective of this study was to test the hypothesis that the body burden of Mn is positively correlated with ADHD symptoms. We also investigated the putative roles of Ca, Fe, Pb, and Hg. We collected shed molars from 266 children (138 boys and 128 girls who lost a tooth between 11 and 13 years of age. The molars were analyzed for metals using ICP-OES. The third grade teacher of each child completed the Teacher’s Disruptive Behavior Disorders Rating Scale (DBD to produce a score for “Total Disruptive Behavior” and subscale scores for “Attention Deficit Hyperactivity Disorder”, Hyperactivity/Impulsivity, Inattention, and Oppositional/Defiant. The mean Mn, Fe, Pb and Ca concentrations found in teeth was 6.1 ± 5.7 µg/g, 22.7 ± 24.1 µg/g, 0.9 ± 1.4 µg/g, and 6.0 × 105 ± 1.6 × 105 µg/g, respectively. Hg was not detected. No significant association was found between Mn and behavioral deficits. Ca was significantly negatively associated, and Pb showed a significant positive association with Hyperactivity/Impulsivity, Inattention, and Oppositional/Defiant Disorders. These findings call into question the putative independent association of manganese exposure and behavioral deficits in children, when the balance of other metallic burden, particularly Ca and Pb burdens play significant roles.

  19. Budget Deficits Effects on Economic Growth

    OpenAIRE

    L.C.Risti; C. Nicolaescu; D.Tăgăduan

    2013-01-01

    The budget deficit can not be analyzed autarchically, as it affects all the macroeconomic processes and, is itself influenced by all other macroeconomic indicators. Most analyses and studies on public finance and budget balance measure the impact that budgetary deficits accumulation has on economy. Therefore, the present paper aims at following and analyzing the mutual impact between budget deficit and another economic macro indicator, namely the economic growth.

  20. The contribution of executive skills to reading comprehension.

    Science.gov (United States)

    Sesma, Heather Whitney; Mahone, E Mark; Levine, Terry; Eason, Sarah H; Cutting, Laurie E

    2009-05-01

    Although word recognition deficits (WRD) are a known cause of reading comprehension deficits (RCD), other contributions to RCD, including executive function (EF), have not been fully explored. We examined the contribution of EF (working memory and planning), along with attention, decoding, fluency, and vocabulary to reading comprehension in 60 children (including 16 WRD and 10 RCD), ages 9-15 years. After controlling for commonly accepted contributors to reading comprehension (i.e., attention, decoding skills, fluency, and vocabulary), EF continued to make a significant contribution to reading comprehension but not to word recognition skills. These findings highlight the need for consideration of the role of EF in RCD.

  1. Brain region-specific perfluoroalkylated sulfonate (PFSA) and carboxylic acid (PFCA) accumulation and neurochemical biomarker responses in east Greenland polar bears (Ursus maritimus).

    Science.gov (United States)

    Eggers Pedersen, Kathrine; Basu, Niladri; Letcher, Robert; Greaves, Alana K; Sonne, Christian; Dietz, Rune; Styrishave, Bjarne

    2015-04-01

    Perfluoroalkyl substances (PFASs) is a growing class of contaminants in the Arctic environment, and include the established perfluorinated sulfonates (PFSAs; especially perfluorooctane sulfonate (PFOS)) and carboxylic acids (PFCAs). PFSAs and PFCAs of varying chain length have been reported to bioaccumulate in lipid rich tissues of the brain among other tissues such as liver, and can reach high concentrations in top predators including the polar bear. PFCA and PFSA bioaccummulation in the brain has the potential to pose neurotoxic effects and therefore we conducted a study to investigate if variations in neurochemical transmitter systems i.e. the cholinergic, glutaminergic, dopaminergic and GABAergic, could be related to brain-specific bioaccumulation of PFASs in East Greenland polar bears. Nine brain regions from nine polar bears were analyzed for enzyme activity (monoamine oxidase (MAO), acetylcholinesterase (AChE) and glutamine synthetase (GS)) and receptor density (dopamine-2 (D2), muscarinic cholinergic (mAChR) and gamma-butyric acid type A (GABA-A)) along with PFSA and PFCA concentrations. Average brain ∑PFSA concentration was 25ng/g ww where PFOS accounted for 91%. Average ∑PFCA concentration was 88ng/g ww where PFUnDA, PFDoDA and PFTrDA combined accounted for 79%. The highest concentrations of PFASs were measured in brain stem, cerebellum and hippocampus. Correlative analyses were performed both across and within brain regions. Significant positive correlations were found between PFASs and MAO activity in occipital lobe (e.g. ∑PFCA; rp=0.83, p=0.041, n=6) and across brain regions (e.g. ∑PFCA; rp=0.47, p=0.001, ∑PFSA; rp=0.44, p>0.001; n=50). GABA-A receptor density was positively correlated with two PFASs across brain regions (PFOS; rp=0.33, p=0.02 and PFDoDA; rp=0.34, p=0.014; n=52). Significant negative correlations were found between mAChR density and PFASs in cerebellum (e.g. ∑PFCA; rp=-0.95, p=0.013, n=5) and across brain regions (e.g.

  2. Applying Time-sharing technique in a multimodal compact low-power CMOS neurochip for simultaneous neurochemical and action potential recording.

    Science.gov (United States)

    Poustinchi, Mohammad; Stacey, R Greg; Musallam, Sam

    2014-01-01

    Brain is an electrochemical system and recent studies suggest simultaneous measurement of interrelated brain's electrical and neurochemical activity may lead to better understanding of brain function in addition to developing optimal neural prosthetics. By exploiting opamp Time-sharing technique to minimized power dissipation and silicon area, we have fabricated a power efficient implantable CMOS microsystem for simultaneous measurement of Action Potential (AP) and neurotransmitter concentration. Both AP-recording and neurotransmitter sensing subsystems share a single 653 nW amplifier which senses picoscale to microscale current that corresponds to micromolar neurotransmitter concentration and microscale AP voltage. This microsystem is fabricated in CMOS 0.18 μm technology and tested using recorded signals from dorsal premotor cortex (PMd) area of a macaque monkey in our lab.

  3. Lifespan development of the bilateral deficit in a simple reaction time task.

    Science.gov (United States)

    Vieluf, Solveig; Aschersleben, Gisa; Panzer, Stefan

    2017-04-01

    Performing an action at a maximum speed or with a maximum strength simultaneously with two limbs leads to a lower performance than the sum of unimanual performances. This phenomenon is known as bilateral deficit. There is some evidence that the bilateral deficit changes over the lifespan, in a way that children and older adults show lower deficits than young adults. Inverse developmental changes of childrens' and older adults' brain structures connecting both hemispheres, i.e., the corpus callosum, might importantly contribute to this phenomenon. The seemingly similar developments have been observed with different experimental protocols in the different age groups, respectively. To test for similarities and differences in changes of the bilateral deficit at critical periods of the lifespan development of bimanual actions, children, young adults, and older adults performed a simple reaction time task uni- and bimanually. Reaction times and the resulting bilateral deficit, as well as reaction time variability were analyzed. As expected, reaction times were different for the young adults between the uni- and the bimanual task. Children and older adults performed both conditions with similar reaction times. However, a difference in the direction of the %bilateral deficit occurred between the two age groups. The findings demonstrated an absence of the bilateral deficit for children, but not for younger and older adults.

  4. Brain hemispheric differences in the neurochemical effects of lead, prenatal stress, and the combination and their amelioration by behavioral experience.

    Science.gov (United States)

    Cory-Slechta, Deborah A; Weston, Douglas; Liu, Sue; Allen, Joshua L

    2013-04-01

    Brain lateralization, critical to mediation of cognitive functions and to "multitasking," is disrupted in conditions such as attention deficit disorder and schizophrenia. Both low-level lead (Pb) exposure and prenatal stress (PS) have been associated with mesocorticolimbic system-mediated executive-function cognitive and attention deficits. Mesocorticolimbic systems demonstrate significant laterality. Thus, altered brain lateralization could play a role in this behavioral toxicity. This study examined laterality of mesocorticolimbic monoamines (frontal cortex, nucleus accumbens, striatum, midbrain) and amino acids (frontal cortex) in male and female rats subjected to lifetime Pb exposure (0 or 50 ppm in drinking water), PS (restraint stress on gestational days 16-17), or the combination with and without repeated learning behavioral experience. Control males exhibited prominent laterality, particularly in midbrain and also in frontal cortex and striatum; females exhibited less laterality, and this was primarily striatal. Lateralized Pb ± PS induced neurotransmitter changes were assessed only in males because of limited sample sizes of Pb + PS females. In males, Pb ± PS changes occurred in left hemisphere of frontal cortex and right hemisphere of midbrain. Behavioral experience modified the laterality of Pb ± PS-induced neurotransmitter changes in a region-dependent manner. Notably, behavioral experience eliminated Pb ± PS neurotransmitter changes in males. These findings underscore the critical need to evaluate both sexes and brain hemispheres for the mechanistic understanding of sex-dependent differences in neuro- and behavioral toxicity. Furthermore, assessment of central nervous system mechanisms in the absence of behavioral experience, shown here for males, may constitute less relevant models of human health effects.

  5. Poor Reading: A Deficit in Skill-Automatization or a Phonological Deficit?

    Science.gov (United States)

    Wimmer, Heinz; Mayringer, Heinz; Landerl, Karin.

    1998-01-01

    Examines whether the characteristic reading speed impairment of German dyslexic children resulted from a general skill-automatization deficit or a phonological deficit. Tests a dyslexic and nondyslexic group of boys in grade 2. Concludes that difficulties in learning to read are due phonological deficit and not a general skill-automatization…

  6. Timing deficits in attention-deficit/hyperactivity disorder (ADHD) : Evidence from neurocognitive and neuroimaging studies

    NARCIS (Netherlands)

    Noreika, Valdas; Falter, Christine M.; Rubia, Katya

    Relatively recently, neurocognitive and neuroimaging studies have indicated that individuals with attention-deficit/hyperactivity disorder (ADHD) may have deficits in a range of timing functions and their underlying neural networks. Despite this evidence, timing deficits in ADHD are still somewhat

  7. Unique Behavioral and Neurochemical Effects Induced by Repeated Adolescent Consumption of Caffeine-Mixed Alcohol in C57BL/6 Mice.

    Science.gov (United States)

    Robins, Meridith T; Lu, Julie; van Rijn, Richard M

    2016-01-01

    The number of highly caffeinated products has increased dramatically in the past few years. Among these products, highly caffeinated energy drinks are the most heavily advertised and purchased, which has resulted in increased incidences of co-consumption of energy drinks with alcohol. Despite the growing number of adolescents and young adults reporting caffeine-mixed alcohol use, knowledge of the potential consequences associated with co-consumption has been limited to survey-based results and in-laboratory human behavioral testing. Here, we investigate the effect of repeated adolescent (post-natal days P35-61) exposure to caffeine-mixed alcohol in C57BL/6 mice on common drug-related behaviors such as locomotor sensitivity, drug reward and cross-sensitivity, and natural reward. To determine changes in neurological activity resulting from adolescent exposure, we monitored changes in expression of the transcription factor ΔFosB in the dopaminergic reward pathway as a sign of long-term increases in neuronal activity. Repeated adolescent exposure to caffeine-mixed alcohol exposure induced significant locomotor sensitization, desensitized cocaine conditioned place preference, decreased cocaine locomotor cross-sensitivity, and increased natural reward consumption. We also observed increased accumulation of ΔFosB in the nucleus accumbens following repeated adolescent caffeine-mixed alcohol exposure compared to alcohol or caffeine alone. Using our exposure model, we found that repeated exposure to caffeine-mixed alcohol during adolescence causes unique behavioral and neurochemical effects not observed in mice exposed to caffeine or alcohol alone. Based on similar findings for different substances of abuse, it is possible that repeated exposure to caffeine-mixed alcohol during adolescence could potentially alter or escalate future substance abuse as means to compensate for these behavioral and neurochemical alterations.

  8. Unique Behavioral and Neurochemical Effects Induced by Repeated Adolescent Consumption of Caffeine-Mixed Alcohol in C57BL/6 Mice.

    Directory of Open Access Journals (Sweden)

    Meridith T Robins

    Full Text Available The number of highly caffeinated products has increased dramatically in the past few years. Among these products, highly caffeinated energy drinks are the most heavily advertised and purchased, which has resulted in increased incidences of co-consumption of energy drinks with alcohol. Despite the growing number of adolescents and young adults reporting caffeine-mixed alcohol use, knowledge of the potential consequences associated with co-consumption has been limited to survey-based results and in-laboratory human behavioral testing. Here, we investigate the effect of repeated adolescent (post-natal days P35-61 exposure to caffeine-mixed alcohol in C57BL/6 mice on common drug-related behaviors such as locomotor sensitivity, drug reward and cross-sensitivity, and natural reward. To determine changes in neurological activity resulting from adolescent exposure, we monitored changes in expression of the transcription factor ΔFosB in the dopaminergic reward pathway as a sign of long-term increases in neuronal activity. Repeated adolescent exposure to caffeine-mixed alcohol exposure induced significant locomotor sensitization, desensitized cocaine conditioned place preference, decreased cocaine locomotor cross-sensitivity, and increased natural reward consumption. We also observed increased accumulation of ΔFosB in the nucleus accumbens following repeated adolescent caffeine-mixed alcohol exposure compared to alcohol or caffeine alone. Using our exposure model, we found that repeated exposure to caffeine-mixed alcohol during adolescence causes unique behavioral and neurochemical effects not observed in mice exposed to caffeine or alcohol alone. Based on similar findings for different substances of abuse, it is possible that repeated exposure to caffeine-mixed alcohol during adolescence could potentially alter or escalate future substance abuse as means to compensate for these behavioral and neurochemical alterations.

  9. Pragmatic comprehension deficit in Parkinson's disease.

    Science.gov (United States)

    Holtgraves, Thomas; McNamara, Patrick

    2010-04-01

    Recognizing the specific speech act (Searle, 1969) that a speaker performs with an utterance is a fundamental feature of pragmatic competence. However, little is known about neurocognitive mediation of speech act comprehension. The present research examined the extent to which people with Parkinson's disease (PD) comprehend specific speech acts. In the first experiment, participants read conversational utterances and then performed a lexical decision task (decide whether a target string of letters was a word). Consistent with past research, nonimpaired participants performed this task more quickly when the target string was the speech act associated with the preceding utterance. In contrast, people with PD did not demonstrate this effect, suggesting that speech act activation is slowed or is not an automatic component of comprehension for people with PD. In a second study, participants were given unlimited time to indicate their recognition of the speech act performed with an utterance. PD participants were significantly poorer at this task than were control participants. We conclude that a previously undocumented language disorder exists in PD and that this disorder involves a selective deficit in speech act comprehension. Frontostriatal systems (the systems impaired in PD) likely contribute to normal speech act comprehension.

  10. Mindfulness and Attention Deficit Hyperactivity Disorder

    Science.gov (United States)

    Smalley, Susan L.; Loo, Sandra K.; Hale, T. Sigi; Shrestha, Anshu; McGough, James; Flook, Lisa; Reise, Steven

    2010-01-01

    Attention Deficit Hyperactivity Disorder (ADHD) is a disorder characterized by attentional difficulties. Mindfulness is a receptive attention to present experience. Both ADHD and mindfulness are associated with attention and personality. This study tests whether individuals with ADHD have lower mindfulness scores than controls and, if true, whether personality contributes to these differences. 105 adults (half with ADHD) were assessed for mindfulness, using the Kentucky Inventory of Mindfulness Skills, and personality, using the Tridimensional Character Inventory. Individuals with ADHD report themselves as less mindful than non-ADHD controls and more novelty-seeking, less self-directed, and more self-transcendent. Mindfulness is negatively associated with ADHD and positively associated with self-directedness and self-transcendence. Analyses of subscales of mindfulness suggest that ADHD is associated most with the ‘Acting in Awareness’ dimension perhaps due to shared items reflecting attentional variability. The current findings support that a large portion of variability in trait mindfulness can be explained by ADHD status and personality traits of self-directedness and self-transcendence. It further suggests that interventions that increase mindfulness might improve symptoms of ADHD and increase self-directedness and/or self-transcendence. PMID:19681107

  11. Attention-Deficit/Hyperactivity Disorder.

    Science.gov (United States)

    Bokor, Gyula; Anderson, Peter D

    2014-08-01

    Attention-deficit/hyperactivity disorder (ADHD) is a neurobiological condition of childhood onset with the hallmarks of inattention, impulsivity, and hyperactivity. Inattention includes excessive daydreaming, disorganization, and being easily distracted. Impulsivity manifests as taking an action before fully thinking of the consequences. Hyperactivity includes an excessive rate of speech and motor activity. Complications of ADHD include academic failure, low self-esteem, poor work performance, substance abuse, criminal justice issues, and social problems. ADHD is predominately due to decreased activity in the frontal lobe. Dopamine and norepinephrine are the main neurotransmitters involved in the pathophysiology of ADHD. Pharmacological treatment of ADHD includes psychostimulants, norepinephrine reuptake inhibitors, α2 agonists, bupropion, and monoamine oxidase inhibitors. The most effective medications are the psychostimulants. Nonpharmacological treatment of ADHD includes coaching, providing structure, academic accommodations, and work accommodations. © The Author(s) 2014.

  12. Gendering attention deficit hyperactivity disorder: a discursive analysis of UK newspaper stories.

    Science.gov (United States)

    Horton-Salway, Mary

    2013-08-01

    Discursive psychology is used to study the gendering of attention deficit hyperactivity disorder in UK national newspapers in the period of 2009-2011. The analysis examines how gendering is embedded in causal attributions and identity constructions. Attention deficit hyperactivity disorder is portrayed as a predominantly male phenomenon with representations of attention deficit hyperactivity disorder being gendered through extreme stories about victims, villains or heroes that depict boys and men as marginalised, exceptional or dangerous. There is also a focus on mothers as the spokespersons and caretakers for parenting and family health while fathers are rendered more invisible. This contributes to our understanding of how attention deficit hyperactivity disorder is constructed in the media using a range of gendered representations that draw on cultural stereotypes familiar in Western societies.

  13. attention deficit hyperactivity disorder intervention: strategies

    African Journals Online (AJOL)

    Elizabeth

    Abstract. This paper addresses attention deficit hyperactivity disorder intervention strategies for primary school teachers. Wrong labelling of children with attention deficit hyperactivity disorder has given rise to this paper. Hitherto not much attention has been given to the pupils who manifest symptoms of this chronic.

  14. Attention Deficit Disorder (ADHD): Primary school teachers ...

    African Journals Online (AJOL)

    Hennie

    A self-administered questionnaire, the Knowledge of Attention-Deficit Disorder Scale. (KADDS), which measures the ... Attention Deficit Disorder (ADHD) is characterised by“a chronic and pervasive pattern of developmentally inappropriate levels of ..... (86.9%), communication as intervention (86.4%), academic and social ...

  15. Measuring Working Memory Deficits in Aphasia

    Science.gov (United States)

    Mayer, Jamie F.; Murray, Laura L.

    2012-01-01

    Purpose: Many adults with aphasia demonstrate concomitant deficits in working memory (WM), but such deficits are difficult to quantify because of a lack of validated measures as well as the complex interdependence between language and WM. We examined the feasibility, reliability, and internal consistency of an "n"-back task for…

  16. Neurobehavioral deficits in progressive experimental hydrocephalus ...

    African Journals Online (AJOL)

    Hydrocephalus is usually associated with functional deficits which can be assessed by neurobehavioral tests. This study characterizes the neurobehavioral deficits occurring with increasing duration and severity of ventriculomegaly in an experimental neonatal hydrocephalic rat model. Hydrocephalus was induced in three ...

  17. Deficits in Emotional Clarity and Vulnerability to Peer Victimization and Internalizing Symptoms Among Early Adolescents.

    Science.gov (United States)

    Hamilton, Jessica L; Kleiman, Evan M; Rubenstein, Liza M; Stange, Jonathan P; Flynn, Megan; Abramson, Lyn Y; Alloy, Lauren B

    2016-01-01

    Peer victimization is a significant risk factor for a range of negative outcomes during adolescence, including depression and anxiety. Recent research has evaluated individual characteristics that heighten the risk of experiencing peer victimization. However, the role of emotional clarity, or the ability to understand one's emotions, in being the target of peer victimization remains unclear. Thus, the present study evaluated whether deficits in emotional clarity increased the risk of experiencing peer victimization, particularly among adolescent girls, which, in turn, contributed to prospective levels of depressive and anxiety symptoms. In the present study, 355 early adolescents (ages 12-13; 53% female; 51% African American) who were part of the Adolescent Cognition and Emotion project completed measures of emotional clarity, depressive symptoms, and anxiety symptoms at baseline, and measures of peer victimization, depressive symptoms, and anxiety symptoms at follow-up. Moderation analyses indicated that deficits in emotional clarity predicted greater peer victimization among adolescent girls, but not adolescent boys. Moderated mediation analyses revealed that deficits in emotional clarity contributed to relational peer victimization, which, in turn, predicted prospective levels of depressive and anxiety symptoms among adolescent girls, but not boys. These findings indicate that deficits in emotional clarity represent a significant risk factor for adolescent girls to experience relational peer victimization, which, in turn, contributed to prospective levels of internalizing symptoms. Thus, prevention programs should target deficits in emotional clarity to prevent peer victimization and subsequent internalizing symptoms among adolescent girls.

  18. Familial Liability to Epilepsy and Attention-Deficit/Hyperactivity Disorder

    DEFF Research Database (Denmark)

    Brikell, Isabell; Ghirardi, Laura; D'Onofrio, Brian M

    2018-01-01

    BACKGROUND: Epilepsy and attention-deficit/hyperactivity disorder (ADHD) are strongly associated; however, the underlying factors contributing to their co-occurrence remain unclear. A shared genetic liability has been proposed as one possible mechanism. Therefore, our goal in this study was to in......BACKGROUND: Epilepsy and attention-deficit/hyperactivity disorder (ADHD) are strongly associated; however, the underlying factors contributing to their co-occurrence remain unclear. A shared genetic liability has been proposed as one possible mechanism. Therefore, our goal in this study...... was to investigate the familial coaggregation of epilepsy and ADHD and to estimate the contribution of genetic and environmental risk factors to their co-occurrence. METHODS: We identified 1,899,654 individuals born between 1987 and 2006 via national Swedish registers and linked each individual to his or her...... biological relatives. We used logistic regression to estimate the association between epilepsy and ADHD within individual and across relatives. Quantitative genetic modeling was used to decompose the cross-disorder covariance into genetic and environmental factors. RESULTS: Individuals with epilepsy had...

  19. Glucocorticoid therapy-induced memory deficits: acute versus chronic effects.

    Science.gov (United States)

    Coluccia, Daniel; Wolf, Oliver T; Kollias, Spyros; Roozendaal, Benno; Forster, Adrian; de Quervain, Dominique J-F

    2008-03-26

    Conditions with chronically elevated glucocorticoid levels are usually associated with declarative memory deficits. Considerable evidence suggests that long-term glucocorticoid exposure may cause cognitive impairment via cumulative and long-lasting influences on hippocampal function and morphology. However, because elevated glucocorticoid levels at the time of retention testing are also known to have direct impairing effects on memory retrieval, it is possible that such acute hormonal influences on retrieval processes contribute to the memory deficits found with chronic glucocorticoid exposure. To investigate this issue, we examined memory functions and hippocampal volume in 24 patients with rheumatoid arthritis who were treated either chronically (5.3 +/- 1.0 years, mean +/- SE) with low to moderate doses of prednisone (7.5 +/- 0.8 mg, mean +/- SE) or without glucocorticoids. In both groups, delayed recall of words learned 24 h earlier was assessed under conditions of either elevated or basal glucocorticoid levels in a double-blind, placebo-controlled crossover design. Although the findings in this patient population did not provide evidence for harmful effects of a history of chronic prednisone treatment on memory performance or hippocampal volume per se, acute prednisone administration 1 h before retention testing to either the steroid or nonsteroid group impaired word recall. Thus, these findings indicate that memory deficits observed under chronically elevated glucocorticoid levels result, at least in part, from acute and reversible glucocorticoid effects on memory retrieval.

  20. Theory of mind deficits in bipolar affective disorder.

    Science.gov (United States)

    Kerr, Natalie; Dunbar, Robin I M; Bentall, Richard P

    2003-02-01

    Bipolar affective disorder patients often show cognitive deficits that are similar to those found in schizophrenia patients. Theory of mind (the ability to understand others' mental states) is compromised in currently ill schizophrenia patients. This study aimed to establish whether similar deficits are found in bipolar patients. We measured theory of mind ability in 20 bipolar-manic patients, 15 bipolar-depressed patients, 13 bipolar patients in remission and 15 normal controls. The task, which controlled for memory and comprehension, had previously been used in a study of schizophrenia patients. Impaired performance on theory of mind was found for both bipolar-depressed and bipolar-manic patients, even when memory was controlled for. No impairment was observed in the remitted patients. The manic patients scored lower than the remitted patients on a brief measure of intelligence; no other group differences in IQ were significant. Theory of mind deficits are found in currently symptomatic bipolar patients. These findings add to growing evidence that common mechanisms may contribute to bipolar affective disorder and schizophrenia.

  1. Hippocampus and amygdala morphology in attention-deficit/hyperactivity disorder

    DEFF Research Database (Denmark)

    Plessen, Kerstin J; Bansal, Ravi; Zhu, Hongtu

    2006-01-01

    of disturbances in the perception of time, temporal processing (eg, delay aversion), and stimulus seeking associated with ADHD. Disrupted connections between the amygdala and orbitofrontal cortex may contribute to behavioral disinhibition. Our findings suggest involvement of the limbic system......CONTEXT: Limbic structures are implicated in the genesis of attention-deficit/hyperactivity disorder (ADHD) by the presence of mood and cognitive disturbances in affected individuals and by elevated rates of mood disorders in family members of probands with ADHD. OBJECTIVE: To study the morphology...

  2. Color naming deficits and attention-deficit/hyperactivity disorder: A retinal dopaminergic hypothesis

    Directory of Open Access Journals (Sweden)

    Tannock Rosemary

    2006-01-01

    Full Text Available Abstract Background Individuals with Attention-Deficit/Hyperactive Disorder (ADHD have unexplained difficulties on tasks requiring speeded processing of colored stimuli. Color vision mechanisms, particularly short-wavelength (blue-yellow pathways, are highly sensitive to various diseases, toxins and drugs that alter dopaminergic neurotransmission. Thus, slow color processing might reflect subtle impairments in the perceptual encoding stage of stimulus color, which arise from hypodopaminergic functioning. Presentation of hypotheses 1 Color perception of blue-yellow (but not red-green stimuli is impaired in ADHD as a result of deficient retinal dopamine; 2 Impairments in the blue-yellow color mechanism in ADHD contribute to poor performance on speeded color naming tasks that include a substantial proportion of blue-yellow stimuli; and 3 Methylphenidate increases central dopamine and is also believed to increase retinal dopamine, thereby normalizing blue-yellow color perception, which in turn improves performance on the speeded color naming tasks. Testing the hypothesis Requires three approaches, including:1 direct assessment of color perception in individuals with ADHD to determine whether blue-yellow color perception is selectively impaired; 2 determination of relationship between performance on neuropsychological tasks requiring speeded color processing and color perception; and 3 randomized, controlled pharmacological intervention with stimulant medication to examine the effects of enhancing central dopamine on color perception and task performance Implications of hypothesis If substantiated, the findings of color perception problems would necessitate a re-consideration of current neuropsychological models of attention-deficit/hyperactivity disorder, guide psycho-education, academic instruction, and require consideration of stimulus color in many of the widely used neuropsychological tests.

  3. Attenuation by a sigma1 (sigma1) receptor agonist of the learning and memory deficits induced by a prenatal restraint stress in juvenile rats.

    Science.gov (United States)

    Meunier, Johann; Gué, Michèle; Récasens, Max; Maurice, Tangui

    2004-06-01

    1. Stress during pregnancy results in complex neurochemical and behavioral alterations throughout the offspring lifetime. We here examined the impact of prenatal stress (PS) on memory functions in male and female offspring and report the efficacy of a selective sigma(1) (sigma(1)) receptor agonist, igmesine, in alleviating the observed deficits. 2. Dams received an unpredictable 90-min duration restraint stress from gestational day E17 to E20. Learning was examined in offspring between day P24 and P36 using spontaneous alternation in the Y-maze, delayed alternation in the T-maze, water-maze learning and passive avoidance. 3. Both male and female PS rats showed impairments of spontaneous and delayed alternation performances. Acquisition of a fixed platform position in the water-maze was unchanged in PS rats, but the probe test revealed a diminution of time spent in the training quadrant. Acquisition of a daily changing platform position demonstrated impaired working memory for male and female PS rats. Finally, passive avoidance deficits were observed. 4. Pretreatment with the selective sigma(1) agonist igmesine (1-10 mg x kg(-1) i.p.) reversed the PS-induced learning deficits in offspring rats for each test. The sigma(1) antagonist BD1063 failed to affect performances alone but blocked the igmesine effect, confirming the involvement of the sigma(1) receptor. 5. PS thus induces delayed memory deficits, affecting spatial and nonspatial, short- and long-term memories in juvenile male and female offspring rats. Activation of the sigma(1) neuromodulatory receptor allows a significant recovery of the memory functions in PS rats.

  4. Attenuation by a sigma1 (σ1) receptor agonist of the learning and memory deficits induced by a prenatal restraint stress in juvenile rats

    Science.gov (United States)

    Meunier, Johann; Gué, Michèle; Récasens, Max; Maurice, Tangui

    2004-01-01

    Stress during pregnancy results in complex neurochemical and behavioral alterations throughout the offspring lifetime. We here examined the impact of prenatal stress (PS) on memory functions in male and female offspring and report the efficacy of a selective sigma1 (σ1) receptor agonist, igmesine, in alleviating the observed deficits. Dams received an unpredictable 90-min duration restraint stress from gestational day E17 to E20. Learning was examined in offspring between day P24 and P36 using spontaneous alternation in the Y-maze, delayed alternation in the T-maze, water-maze learning and passive avoidance. Both male and female PS rats showed impairments of spontaneous and delayed alternation performances. Acquisition of a fixed platform position in the water-maze was unchanged in PS rats, but the probe test revealed a diminution of time spent in the training quadrant. Acquisition of a daily changing platform position demonstrated impaired working memory for male and female PS rats. Finally, passive avoidance deficits were observed. Pretreatment with the selective σ1 agonist igmesine (1–10 mg kg−1 i.p.) reversed the PS-induced learning deficits in offspring rats for each test. The σ1 antagonist BD1063 failed to affect performances alone but blocked the igmesine effect, confirming the involvement of the σ1 receptor. PS thus induces delayed memory deficits, affecting spatial and nonspatial, short- and long-term memories in juvenile male and female offspring rats. Activation of the σ1 neuromodulatory receptor allows a significant recovery of the memory functions in PS rats. PMID:15205309

  5. Different underlying mechanisms for deficits in concept formation in dementia.

    Science.gov (United States)

    Giovannetti, T; Lamar, M; Cloud, B S; Swenson, R; Fein, D; Kaplan, E; Libon, D J

    2001-08-01

    We investigated the different mechanisms that may underlie deficits in verbal concept formation among patients with Alzheimer's disease (AD) and ischaemic vascular dementia (IVD) associated with periventricular and deep white matter alterations. Concept formation was assessed with the WAIS-R Similarities subtest (SIM). Two types of errors were re-coded from the 0-point responses as scored by the WAIS-R manual. In set errors (e.g., dog-lion "they're alive") were coded when patients reported a very vague superordinate concept for the word pair. Out of set responses (e.g., dog-lion "the lion roars and the dog barks") were coded when a response was clearly out of mental set, i.e., when participants were unable to provide a superordinate concept for the word pair. Between-group comparisons demonstrated no difference in SIM test performance according to the scoring system described in the WAIS-R manual. Nonetheless, AD patients produced a greater proportion of in set errors, while IVD patients produced a greater proportion of out of set errors. Out of set errors were highly associated with measures of executive function, while in set errors were associated with measures related to delayed recognition memory and semantic intrusion errors. We conclude that the underlying deficits that contribute to poor concept formation differ between AD and IVD patients. In IVD impaired concept formation is related to deficits in the executive systems necessary to monitor responses and sustain mental set. In AD, by contrast, the deficit appears to be secondary to impaired verbal response selection.

  6. Dissociations between developmental dyslexias and attention deficits

    Science.gov (United States)

    Lukov, Limor; Friedmann, Naama; Shalev, Lilach; Khentov-Kraus, Lilach; Shalev, Nir; Lorber, Rakefet; Guggenheim, Revital

    2014-01-01

    We examine whether attention deficits underlie developmental dyslexia, or certain types of dyslexia, by presenting double dissociations between the two. We took into account the existence of distinct types of dyslexia and of attention deficits, and focused on dyslexias that may be thought to have an attentional basis: letter position dyslexia (LPD), in which letters migrate within words, attentional dyslexia (AD), in which letters migrate between words, neglect dyslexia, in which letters on one side of the word are omitted or substituted, and surface dyslexia, in which words are read via the sublexical route. We tested 110 children and adults with developmental dyslexia and/or attention deficits, using extensive batteries of reading and attention. For each participant, the existence of dyslexia and the dyslexia type were tested using reading tests that included stimuli sensitive to the various dyslexia types. Attention deficit and its type was established through attention tasks assessing sustained, selective, orienting, and executive attention functioning. Using this procedure, we identified 55 participants who showed a double dissociation between reading and attention: 28 had dyslexia with normal attention and 27 had attention deficits with normal reading. Importantly, each dyslexia with suspected attentional basis dissociated from attention: we found 21 individuals with LPD, 13 AD, 2 neglect dyslexia, and 12 surface dyslexia without attention deficits. Other dyslexia types (vowel dyslexia, phonological dyslexia, visual dyslexia) also dissociated from attention deficits. Examination of 55 additional individuals with both a specific dyslexia and a certain attention deficit found no attention function that was consistently linked with any dyslexia type. Specifically, LPD and AD dissociated from selective attention, neglect dyslexia dissociated from orienting, and surface dyslexia dissociated from sustained and executive attention. These results indicate that

  7. Sleep deficits but no metabolic deficits in premanifest Huntington's disease

    Science.gov (United States)

    Panin, Francesca; Goodman, Anna O. G.; Lazic, Stanley E.; Lazar, Zsolt I.; Mason, Sarah L.; Rogers, Lorraine; Murgatroyd, Peter R.; Watson, Laura P. E.; Singh, Priya; Borowsky, Beth; Shneerson, John M.; Barker, Roger A.

    2015-01-01

    Objective Huntington disease (HD) is a fatal autosomal dominant, neurodegenerative condition characterized by progressively worsening motor and nonmotor problems including cognitive and neuropsychiatric disturbances, along with sleep abnormalities and weight loss. However, it is not known whether sleep disturbances and metabolic abnormalities underlying the weight loss are present at a premanifest stage. Methods We performed a comprehensive sleep and metabolic study in 38 premanifest gene carrier individuals and 36 age‐ and sex‐matched controls. The study consisted of 2 weeks of actigraphy at home, 2 nights of polysomnography and multiple sleep latency tests in the laboratory, and body composition assessment using dual energy x‐ray absorptiometry scanning with energy expenditure measured over 10 days at home by doubly labeled water and for 36 hours in the laboratory by indirect calorimetry along with detailed cognitive and clinical assessments. We performed a principal component analyses across all measures within each studied domain. Results Compared to controls, premanifest gene carriers had more disrupted sleep, which was best characterized by a fragmented sleep profile. These abnormalities, as well as a theta power (4–7Hz) decrease in rapid eye movement sleep, were associated with disease burden score. Objectively measured sleep problems coincided with the development of cognitive, affective, and subtle motor deficits and were not associated with any metabolic alterations. Interpretation The results show that among the earliest abnormalities in premanifest HD is sleep disturbances. This raises questions as to where the pathology in HD begins and also whether it could drive some of the early features and even possibly the pathology. Ann Neurol 2015;78:630–648 PMID:26224419

  8. Postural control deficits identify lingering post-concussion neurological deficits

    Directory of Open Access Journals (Sweden)

    Thomas A. Buckley

    2016-03-01

    Full Text Available Concussion, or mild traumatic brain injury, incidence rates have reached epidemic levels and impaired postural control is a cardinal symptom. The purpose of this review is to provide an overview of the linear and non-linear assessments of post-concussion postural control. The current acute evaluation for concussion utilizes the subjective balance error scoring system (BESS to assess postural control. While the sensitivity of the overall test battery is high, the sensitivity of the BESS is unacceptably low and, with repeat administration, is unable to accurately identify recovery. Sophisticated measures of postural control, utilizing traditional linear assessments, have identified impairments in postural control well beyond BESS recovery. Both assessments of quiet stance and gait have identified lingering impairments for at least 1 month post-concussion. Recently, the application of non-linear metrics to concussion recovery have begun to receive limited attention with the most commonly utilized metric being approximate entropy (ApEn. ApEn, most commonly in the medial-lateral plane, has successfully identified impaired postural control in the acute post-concussion timeframe even when linear assessments of instrumented measures are equivalent to healthy pre-injury values; unfortunately these studies have not gone beyond the acute phase of recovery. One study has identified lingering deficits in postural control, utilizing Shannon and Renyi entropy metrics, which persist at least through clinical recovery and return to participation. Finally, limited evidence from two studies suggest that individuals with a previous history of a single concussion, even months or years prior, may display altered ApEn metrics. Overall, non-linear metrics provide a fertile area for future study to further the understanding of postural control impairments acutely post-concussion and address the current challenge of sensitive identification of recovery.

  9. Association of intracortical inhibition with social cognition deficits in schizophrenia: Findings from a transcranial magnetic stimulation study.

    Science.gov (United States)

    Mehta, Urvakhsh Meherwan; Thirthalli, Jagadisha; Basavaraju, Rakshathi; Gangadhar, Bangalore N

    2014-09-01

    Abnormal cortical-inhibition has been hypothesized to underlie social-cognition deficits in schizophrenia. Studies using transcranial magnetic stimulation (TMS) as a neurophysiological probe have demonstrated cortical-inhibition deficits in this group. We compared TMS-measured short- and long-interval intracortical-inhibition (SICI & LICI) in antipsychotic-naïve (n=33) and medicated (n=21) schizophrenia patients and in healthy comparison subjects (n=45). We also studied the association between cortical-inhibition and social-cognition deficits in the patients. Antipsychotic-naïve patients had significant deficits in SICI (i.e., less inhibitory response). In this group, SICI had significant inverse correlations with emotion processing and a global social-cognition score. Impaired intracortical-inhibition may thus contribute to social-cognition deficits in schizophrenia. Copyright © 2014 Elsevier B.V. All rights reserved.

  10. Deficit Limits, Budget Rules, and Fiscal Policy

    OpenAIRE

    Paolo Manasse

    2005-01-01

    The paper presents a simple model for discussing the effects of deficit limits and budget rules on fiscal policy. I find that limits on deficit- output ratios provide incentives to implement procyclical policies when the economy is in intermediate states, and countercyclical policies only in very “good” and very “bad” economic times. As a result, fiscal “reaction functions” are not monotonically related to the state of the economy. Deficit limits are found to exert discipline only provided th...

  11. Visual imagery deficits, impaired strategic retrieval, or memory loss: disentangling the nature of an amnesic person's autobiographical memory deficit.

    Science.gov (United States)

    Rosenbaum, R Shayna; McKinnon, Margaret C; Levine, Brian; Moscovitch, Morris

    2004-01-01

    Conclusions about the duration of hippocampal contributions to our autobiographical record of personal episodes have come under intense scrutiny in recent years. Interpretation is complicated by such factors as extent and site of lesions as well as test sensitivity. We describe the case of an amnesic person, K.C., with large, bilateral hippocampal lesions who figured prominently in the development of theories of remote memory due to his severely impoverished autobiographical memory extending across his entire lifetime. However, the presence of lesions in higher-order visual cortex raises the possibility that K.C.'s retrograde autobiographical amnesia is mediated by loss of long-term visual images, whereas widespread frontal lesions suggest that his impairment may relate to deficits in strategic retrieval rather than storage. Normal performance on an extensive battery of visual imagery tests refutes the imagery loss interpretation. To test for deficits in strategic retrieval, we used a more formal autobiographical memory test requiring generation of personal events under varying levels of retrieval support. However, even with rigorous contextual prompting, K.C. produced few pre-injury recollections; all were schematic, lacking the richness of detail produced by control participants, raising doubt that his deficit is one of retrieval. Findings are discussed in the context of theories concerning the duration of hippocampal-neocortical interactions in supporting autobiographical re-experiencing. The approach we used to investigate the effects of different lesions on memory provides a framework for dealing with other patients who present with an interesting functional deficit whose neuroanatomical source is difficult to specify due to widespread lesions.

  12. Early Paradoxical Increase of Dopamine: A Neurochemical Study of Olfactory Bulb in Asymptomatic and Symptomatic MPTP Treated Monkeys

    Science.gov (United States)

    Pifl, Christian; Reither, Harald; del Rey, Natalia Lopez-Gonzalez; Cavada, Carmen; Obeso, Jose A.; Blesa, Javier

    2017-01-01

    Parkinson’s disease (PD) is a neurodegenerative disease with both motor and non-motor manifestations. Hyposmia is one of the early non-motor symptoms, which can precede motor symptoms by several years. The relationship between hyposmia and PD remains elusive. Olfactory bulb (OB) pathology shows an increased number of olfactory dopaminergic cells, protein aggregates and dysfunction of neurotransmitter systems. In this study we examined tissue levels of dopamine (DA) and serotonin (5-hydroxytryptamine, 5-HT) and their metabolites, of noradrenaline (NA) and of the amino acid neurotransmitters aspartate, glutamate, taurine and γ-aminobutyric acid in OBs of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treated Macaca fascicularis in different stages, including monkeys who were always asymptomatic, monkeys who recovered from mild parkinsonian signs, and monkeys with stable moderate or severe parkinsonism. DA was increased compared to controls, while neither NA and 5-HT nor the amino acid neurotransmitters were significantly changed. Furthermore, DA increased before stable motor deficits appear with +51% in asymptomatic and +96% in recovered monkeys. Unchanged DA metabolites suggest a special metabolic profile of the newly formed DA neurons. Significant correlation of homovanillic acid (HVA) with taurine single values within the four MPTP groups and of aspartate with taurine within the asymptomatic and recovered MPTP groups, but not within the controls suggest interactions in the OB between taurine and the DA system and taurine and the excitatory neurotransmitter triggered by MPTP. This first investigation of OB in various stages after MPTP administration suggests that the DA increase seems to be an early phenomenon, not requiring profound nigrostriatal neurodegeneration or PD symptoms. PMID:28611598

  13. Early Paradoxical Increase of Dopamine: A Neurochemical Study of Olfactory Bulb in Asymptomatic and Symptomatic MPTP Treated Monkeys

    Directory of Open Access Journals (Sweden)

    Christian Pifl

    2017-05-01

    Full Text Available Parkinson’s disease (PD is a neurodegenerative disease with both motor and non-motor manifestations. Hyposmia is one of the early non-motor symptoms, which can precede motor symptoms by several years. The relationship between hyposmia and PD remains elusive. Olfactory bulb (OB pathology shows an increased number of olfactory dopaminergic cells, protein aggregates and dysfunction of neurotransmitter systems. In this study we examined tissue levels of dopamine (DA and serotonin (5-hydroxytryptamine, 5-HT and their metabolites, of noradrenaline (NA and of the amino acid neurotransmitters aspartate, glutamate, taurine and γ-aminobutyric acid in OBs of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP treated Macaca fascicularis in different stages, including monkeys who were always asymptomatic, monkeys who recovered from mild parkinsonian signs, and monkeys with stable moderate or severe parkinsonism. DA was increased compared to controls, while neither NA and 5-HT nor the amino acid neurotransmitters were significantly changed. Furthermore, DA increased before stable motor deficits appear with +51% in asymptomatic and +96% in recovered monkeys. Unchanged DA metabolites suggest a special metabolic profile of the newly formed DA neurons. Significant correlation of homovanillic acid (HVA with taurine single values within the four MPTP groups and of aspartate with taurine within the asymptomatic and recovered MPTP groups, but not within the controls suggest interactions in the OB between taurine and the DA system and taurine and the excitatory neurotransmitter triggered by MPTP. This first investigation of OB in various stages after MPTP administration suggests that the DA increase seems to be an early phenomenon, not requiring profound nigrostriatal neurodegeneration or PD symptoms.

  14. Cerebellar Contribution to Social Cognition.

    Science.gov (United States)

    Hoche, Franziska; Guell, Xavier; Sherman, Janet C; Vangel, Mark G; Schmahmann, Jeremy D

    2016-12-01

    Emotion attribution (EA) from faces is key to social cognition, and deficits in perception of emotions from faces underlie neuropsychiatric disorders in which cerebellar pathology is reported. Here, we test the hypothesis that the cerebellum contributes to social cognition through EA from faces. We examined 57 patients with cerebellar disorders and 57 healthy controls. Thirty-one patients had complex cerebrocerebellar disease (complex cerebrocerebellar disease group (CD)); 26 had disease isolated to cerebellum (isolated cerebellar disease group (ID)). EA was measured with the Reading the Mind in the Eyes test (RMET), and informants were administered a novel questionnaire, the Cerebellar Neuropsychiatric Rating Scale (CNRS). EA was impaired in all patients (CD p social skills (p social skills (CD p social skills and autism spectrum behaviors and experienced psychosocial difficulties on the CNRS. This has relevance for ataxias, the cerebellar cognitive affective/Schmahmann syndrome, and neuropsychiatric disorders with cerebellar pathology.

  15. Cerebellar contribution to social cognition

    Science.gov (United States)

    Hoche, Franziska; Guell, Xavier; Sherman, Janet C.; Vangel, Mark G.; Schmahmann, Jeremy D.

    2015-01-01

    Emotion attribution (EA) from faces is key to social cognition, and deficits in perception of emotions from faces underlie neuropsychiatric disorders in which cerebellar pathology is reported. Here we test the hypothesis that the cerebellum contributes to social cognition through EA from faces. We examined fifty-seven patients with cerebellar disorders and 57 healthy controls. Thirty-one patients had complex cerebrocerebellar disease (CD); 26 had disease isolated to cerebellum (ID). EA was measured with the Reading the Mind in the Eyes task (RMET), and informants were administered a novel questionnaire, the Cerebellar Neuropsychiatric Rating Scale (CNRS). EA was impaired in all patients (CD pcerebellar damage were impaired on an EA task associated with deficient social skills and autism spectrum behaviors, and experienced psychosocial difficulties on the CNRS. This has relevance for ataxias, the cerebellar cognitive affective / Schmahmann syndrome, and neuropsychiatric disorders with cerebellar pathology. PMID:26585120

  16. Do Problems with Information Processing Affect the Process of Psychotherapy for Adults with Learning Disabilities or Attention Deficit/Hyperactivity Disorder?

    Science.gov (United States)

    Cosden, Merith; Patz, Sarah; Smith, Steven

    2009-01-01

    Problems in processing information can affect psychosocial functioning. Psychotherapy can be used to address psychosocial problems; however, the same information-processing problems that contribute to disabilities, such as learning disabilities (LD) or attention deficit/hyperactivity disorder (ADHD), particularly deficits in auditory processing…

  17. Chronic excitotoxicity in the guinea pig cochlea induces temporary functional deficits without disrupting otoacoustic emissions

    Science.gov (United States)

    Le Prell, Colleen G.; Yagi, Masao; Kawamoto, Kohei; Beyer, Lisa A.; Atkin, Graham; Raphael, Yehoash; Dolan, David F.; Bledsoe, Sanford C.; Moody, David B.

    2004-08-01

    Brief cochlear excitotoxicity produces temporary neural swelling and transient deficits in auditory sensitivity; however, the consequences of long-lasting excitotoxic insult have not been tested. Chronic intra-cochlear infusion of the glutamate agonist AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) resulted in functional deficits in the sound-evoked auditory brainstem response, as well as in behavioral measures of hearing. The electrophysiological deficits were similar to those observed following acute infusion of AMPA into the cochlea; however, the concentration-response curve was significantly shifted as a consequence of the slower infusion rate used with chronic cochlear administration. As observed following acute excitotoxic insult, complete functional recovery was evident within 7 days of discontinuing the AMPA infusion. Distortion product otoacoustic emissions were not affected by chronic AMPA infusion, suggesting that trauma to outer hair cells did not contribute to AMPA-induced deficits in acoustic sensitivity. Results from the current experiment address the permanence of deficits induced by chronic (14 day) excitotoxic insult as well as deficits in psychophysical detection of longer duration acoustic signals.

  18. A Weak Association between Traits of Attention-Deficit/Hyperactivity Disorder and Gambling in College Students

    Science.gov (United States)

    Canu, Will H.; Schatz, Nicole K.

    2011-01-01

    Attention-Deficit/Hyperactivity Disorder (ADHD) has been characterized as a comorbidity to pathological gambling (PG). However, contradictory evidence has emerged, and it has not been established whether nonimpulsive features of ADHD (e.g., inattention, hyperactivity) contribute to PG risk, or how robust this relationship is in college samples.…

  19. The Role of Sensory Modulation Deficits and Behavioral Symptoms in a Diagnosis for Early Childhood

    Science.gov (United States)

    Perez-Robles, Ruth; Doval, Eduardo; Jane, Ma Claustre; da Silva, Pedro Caldeira; Papoila, Ana Luisa; Virella, Daniel

    2013-01-01

    To contribute to the validation of the sensory and behavioral criteria for Regulation Disorders of Sensory Processing (RDSP) (DC:0-3R, 2005), this study examined a sample of toddlers in a clinical setting to analyze: (1) the severity of sensory modulation deficits and the behavioral symptoms of RDSP; (2) the associations between sensory and…

  20. Segregation and the Underrepresentation of Blacks and Hispanics in Gifted Education: Social Inequality and Deficit Paradigms

    Science.gov (United States)

    Ford, Donna Y.

    2014-01-01

    This article examines the underrepresentation of African American and Hispanic students in gifted education, proposing that social inequality, deficit thinking, and microaggressions contribute to the inequitable segregated programs. Underrepresentation trends are presented, along with methods for calculating underrepresentation and inequity.…

  1. Peer Victimization among Students with Specific Language Impairment, Attention-Deficit/Hyperactivity Disorder, and Typical Development

    Science.gov (United States)

    Redmond, Sean M.

    2011-01-01

    Purpose: The potential contributions of behavioral and verbal liabilities to social risk were examined by comparing peer victimization levels in children with specific language impairment (SLI) to those in children with attention-deficit/hyperactivity disorder (ADHD) and typically developing (TD) children. Method: Sixty children (age range: 7-8…

  2. Meta-analysis of genome-wide linkage scans of attention deficit hyperactivity disorder

    NARCIS (Netherlands)

    Zhou, Kaixin; Dempfle, Astrid; Arcos-Burgos, Mauricio; Bakker, Steven C; Banaschewski, Tobias; Biederman, Joseph; Buitelaar, Jan; Castellanos, F Xavier; Doyle, Alysa; Ebstein, Richard P; Ekholm, Jenny; Forabosco, Paola; Franke, Barbara; Freitag, Christine; Friedel, Susann; Gill, Michael; Hebebrand, Johannes; Hinney, Anke; Jacob, Christian; Lesch, Klaus Peter; Loo, Sandra K; Lopera, Francisco; McCracken, James T; McGough, James J; Meyer, Jobst; Mick, Eric; Miranda, Ana; Muenke, Maximilian; Mulas, Fernando; Nelson, Stanley F; Nguyen, T Trang; Oades, Robert D; Ogdie, Matthew N; Palacio, Juan David; Pineda, David; Reif, Andreas; Renner, Tobias J; Roeyers, Herbert; Romanos, Marcel; Rothenberger, Aribert; Schäfer, Helmut; Sergeant, Joseph; Sinke, Richard J; Smalley, Susan L; Sonuga-Barke, Edmund; Steinhausen, Hans-Christoph; van der Meulen, Emma; Walitza, Susanne; Warnke, Andreas; Lewis, Cathryn M; Faraone, Stephen V; Asherson, Philip

    2008-01-01

    Genetic contribution to the development of attention deficit hyperactivity disorder (ADHD) is well established. Seven independent genome-wide linkage scans have been performed to map loci that increase the risk for ADHD. Although significant linkage signals were identified in some of the studies,

  3. Extended Attention Span Training System: Video Game Neurotherapy for Attention Deficit Disorder.

    Science.gov (United States)

    Pope, Alan T.; Bogart, Edward H.

    1996-01-01

    Describes the Extended Attention Span Training (EAST) system for modifying attention deficits, which takes the concept of biofeedback one step further by making a video game more difficult as the player's brain waves indicate that attention is waning. Notes contributions of this technology to neuropsychology and neurology, where the emphasis is on…

  4. Visual form-processing deficits in autism.

    Science.gov (United States)

    Spencer, Janine V; O'Brien, Justin M D

    2006-01-01

    People with autism have a number of reported deficits in object recognition and global processing. Is there a low-level spatial integration deficit associated with this? We measured spatial-form-coherence detection thresholds using a Glass stimulus in a field of random dots, and compared performance to a similar motion-coherence task. A coherent visual patch was depicted by dots separated by a rotational transformation in space (form) or space-time (motion). To measure parallel visual integration, stimuli were presented for only 250 ms. We compared detection thresholds for children with autism, children with Asperger syndrome, and a matched control group. Children with autism showed a significant form-coherence deficit and a significant motion-coherence deficit, while the performance of the children with Asperger syndrome did not differ significantly from that of controls on either task.

  5. Focusing on ADHD - Attention Deficit Hyperactivity Disorder

    Science.gov (United States)

    ... Subscribe September 2014 Print this issue Focusing on ADHD Attention Deficit Hyperactivity Disorder En español Send us ... Helps Kids With Cerebral Palsy Wise Choices Managing ADHD Help kids with ADHD stay on top of ...

  6. The Gastric Ganglion of Octopus vulgaris: Preliminary Characterization of Gene- and Putative Neurochemical-Complexity, and the Effect of Aggregata octopiana Digestive Tract Infection on Gene Expression

    Science.gov (United States)

    Baldascino, Elena; Di Cristina, Giulia; Tedesco, Perla; Hobbs, Carl; Shaw, Tanya J.; Ponte, Giovanna; Andrews, Paul L. R.

    2017-01-01

    The gastric ganglion is the largest visceral ganglion in cephalopods. It is connected to the brain and is implicated in regulation of digestive tract functions. Here we have investigated the neurochemical complexity (through in silico gene expression analysis and immunohistochemistry) of the gastric ganglion in Octopus vulgaris and tested whether the expression of a selected number of genes was influenced by the magnitude of digestive tract parasitic infection by Aggregata octopiana. Novel evidence was obtained for putative peptide and non-peptide neurotransmitters in the gastric ganglion: cephalotocin, corticotrophin releasing factor, FMRFamide, gamma amino butyric acid, 5-hydroxytryptamine, molluscan insulin-related peptide 3, peptide PRQFV-amide, and tachykinin–related peptide. Receptors for cholecystokininA and cholecystokininB, and orexin2 were also identified in this context for the first time. We report evidence for acetylcholine, dopamine, noradrenaline, octopamine, small cardioactive peptide related peptide, and receptors for cephalotocin and octopressin, confirming previous publications. The effects of Aggregata observed here extend those previously described by showing effects on the gastric ganglion; in animals with a higher level of infection, genes implicated in inflammation (NFκB, fascin, serpinB10 and the toll-like 3 receptor) increased their relative expression, but TNF-α gene expression was lower as was expression of other genes implicated in oxidative stress (i.e., superoxide dismutase, peroxiredoxin 6, and glutathione peroxidase). Elevated Aggregata levels in the octopuses corresponded to an increase in the expression of the cholecystokininA receptor and the small cardioactive peptide-related peptide. In contrast, we observed decreased relative expression of cephalotocin, dopamine β-hydroxylase, peptide PRQFV-amide, and tachykinin-related peptide genes. A discussion is provided on (i) potential roles of the various molecules in food intake

  7. The Gastric Ganglion of Octopus vulgaris: Preliminary Characterization of Gene- and Putative Neurochemical-Complexity, and the Effect of Aggregata octopiana Digestive Tract Infection on Gene Expression

    Directory of Open Access Journals (Sweden)

    Elena Baldascino

    2017-12-01

    Full Text Available The gastric ganglion is the largest visceral ganglion in cephalopods. It is connected to the brain and is implicated in regulation of digestive tract functions. Here we have investigated the neurochemical complexity (through in silico gene expression analysis and immunohistochemistry of the gastric ganglion in Octopus vulgaris and tested whether the expression of a selected number of genes was influenced by the magnitude of digestive tract parasitic infection by Aggregata octopiana. Novel evidence was obtained for putative peptide and non-peptide neurotransmitters in the gastric ganglion: cephalotocin, corticotrophin releasing factor, FMRFamide, gamma amino butyric acid, 5-hydroxytryptamine, molluscan insulin-related peptide 3, peptide PRQFV-amide, and tachykinin–related peptide. Receptors for cholecystokininA and cholecystokininB, and orexin2 were also identified in this context for the first time. We report evidence for acetylcholine, dopamine, noradrenaline, octopamine, small cardioactive peptide related peptide, and receptors for cephalotocin and octopressin, confirming previous publications. The effects of Aggregata observed here extend those previously described by showing effects on the gastric ganglion; in animals with a higher level of infection, genes implicated in inflammation (NFκB, fascin, serpinB10 and the toll-like 3 receptor increased their relative expression, but TNF-α gene expression was lower as was expression of other genes implicated in oxidative stress (i.e., superoxide dismutase, peroxiredoxin 6, and glutathione peroxidase. Elevated Aggregata levels in the octopuses corresponded to an increase in the expression of the cholecystokininA receptor and the small cardioactive peptide-related peptide. In contrast, we observed decreased relative expression of cephalotocin, dopamine β-hydroxylase, peptide PRQFV-amide, and tachykinin-related peptide genes. A discussion is provided on (i potential roles of the various molecules

  8. SU-F-I-68: Longitudinal Neurochemical Changes On Rat Prefrontal Cortex of Single Prolonged Stress Model by Using Proton Magnetic Resonance Spectroscopy at 9.4T

    Energy Technology Data Exchange (ETDEWEB)

    Lim, S-I; Yoo, C-H [Department of Biomedical Engineering, and Research Institute of Biomedical Engineering, The Catholic University of Korea College of Medicine, Seoul, Seoul (Korea, Republic of); Asan Institute for Life Sciences, Asan Medical Center, Seoul, Seoul (Korea, Republic of); Song, K-H; Choe, B-Y [Department of Biomedical Engineering, and Research Institute of Biomedical Engineering, The Catholic University of Korea College of Medicine, Seoul, Seoul (Korea, Republic of); Woo, D-C [Asan Institute for Life Sciences, Asan Medical Center, Seoul, Seoul (Korea, Republic of)

    2016-06-15

    Purpose: Single prolonged stress (SPS) is an animal model of posttraumatic stress disorder (PTSD). However, it has not been known how PTSD develops from the first exposure to traumatic events and neurochemical differences between acute/single stress and PTSD-triggering stress. Therefore, the object of this study is to determine time-dependent neurochemical changes in prefrontal cortex (PFC) of rats using in vivo proton magnetic resonance spectroscopy (1H-MRS). Methods: Male Sprague-Dawley rats (n=14; body weight=200–220g) were used. The SPS protocol was used in this study. Rats were restrained for 2h and then immediately forced to swim for 20min in water (20–24 Celsius). After a 15-min recuperation period, rats were exposed to ether (using a desiccator) until general anesthesia occurred (<5min). In vivo proton MRS was performed 30min before the SPS (Base), approximately 10min after the SPS (D+0), 3 (D+3) and 7 (D+7) days after SPS to investigate time-dependent changes on metabolites levels in the PFC. Acquisition of in vivo MRS spectra and MRI was conducted at the four time points using 9.4 T Agilent Scanner. Concentration of metabolites was quantified by LCModel. Results: Statistical significance was analyzed using one-way ANOVA with post hoc Tukey HSD tests to assess the metabolite changes in the PFC. The SPS resulted in significant stress-induced differences for 7 days in glutamine (F(3,52)=6.750, P=0.001), choline-containing compounds (F(3,52)=16.442, P=0.000), glutamine/glutamate concentrations (F(3,52)=7.352, P=0.000). Conclusion: PTSD in human is associated with decreased neuronal activity in the PFC. In this study, SPS altered total choline, glutamine levels but not NAA levels in the PFC of the rats. Therefore, for the three stressors and quiescent period of seven days, SPS attenuated excitatory tone and membrane turnover but did not affect neural integrity in the PFC.

  9. Anormalidades neuropatológicas e neuroquímicas no transtorno afetivo bipolar Neuropathological and neurochemical abnormalities in bipolar disorder

    Directory of Open Access Journals (Sweden)

    Benício Noronha Frey

    2004-09-01

    Full Text Available OBJETIVOS: Estudos pós-mortem, farmacológicos, de neuroimagem e em modelos animais têm demonstrado uma possível associação de mecanismos de sinalização intracelular na fisiopatologia do transtorno afetivo bipolar (TAB. Esse trabalho tem como objetivo revisar os achados em neuropatologia e bioquímica celular. MÉTODOS: Foi realizada uma pesquisa ao MEDLINE, entre 1980 e 2003, tendo sido utilizados os unitermos: bipolar disorder, signaling, second messengers e postmortem, além de referências cruzadas dos artigos selecionados. RESULTADOS: uropatológicos demonstraram uma diminuição do número de células neuronais e gliais, principalmente no córtex pré-frontal de pacientes bipolares. Estudos neuroquímicos demonstraram alterações nas vias do AMPc, fosfatidilinositol, Wnt/GSK-3beta e Ca++ intracelular nesses pacientes. CONCLUSÃO: Os achados de alterações neuropatológicas e neuroquímicas no TAB podem estar relacionados com a fisiopatologia deste transtorno e com os efeitos dos estabilizadores de humor. No entanto, mais estudos são necessários para esclarecer o papel das cascatas de sinalização intracelular na patogênese deste transtorno.OBJECTIVES: Postmortem, pharmacological, neuroimaging, and animal model studies have demonstrated a possible association of intracellular signaling mechanisms in the pathophysiology of bipolar disorder. The objective of this paper is to review the findings in neuropathology and cellular biochemistry. METHODS: We performed a MEDLINE research, between 1980-2003, using bipolar disorder, signaling, second messengers, and postmortem as keywords, and cross-references. RESULTS: Neuropathological studies reported a decrease in neuronal and glial cells, mainly in the prefrontal cortex of bipolar patients. Neurochemical studies reported dysfunction in cAMP, phosphoinositide, Wnt/GSK-3b, and intracellular Ca++ pathways in these patients. CONCLUSION: The neuropathological and neurochemical abnormalities

  10. Recognition memory deficits in mild cognitive impairment

    OpenAIRE

    Algarabel González, Salvador; Fuentes, Manuel; Escudero, Joaquín; Pitarque, Alfonso; Peset, Vicente; Mazón Herrero, José Francisco; Meléndez Moral, Juan Carlos

    2012-01-01

    There is no agreement on the pattern of recognition memory deficits characteristic of patients diagnosed with mild cognitive impairment (Mel). Whereas lower performance in recollection is the hallmark of Mel, there is a strong controversy about possible deficits in familiarity estimates when using recognition memory tasks. The aim of this research is to shed Iight on the pattern of responding in recollection and familiarity in MCl. Five groups of participants were tested. The main participant...

  11. Neuropsychological deficits in patients with Lyme borreliosis

    OpenAIRE

    Katja Pruša

    2001-01-01

    Slovenia is an endemic area for Lyme borreliosis, a disease that affects many organic systems. Decline in cognitive abilities and emotional changes can appear in acute and chronic stage of the disease beside somatic difficulties. Early antibiotic therapy is of great importance in recovery. Attention and concentration deficits, memory deficits, impaired executive functioning, depression and other symptoms reduce work efficiency and life quality of people with Lyme borreliosis. Neuropsychologic...

  12. Dissociations between developmental dyslexias and attention deficits

    Directory of Open Access Journals (Sweden)

    Limor eLukov

    2015-01-01

    Full Text Available We examine whether attention deficits underlie developmental dyslexia, or certain types of dyslexia, by presenting double dissociations between the two. We took into account the existence of distinct types of dyslexia and of attention deficits, and focused on dyslexias that may be thought to have an attentional basis: letter position dyslexia (LPD, in which letters migrate within words, attentional dyslexia (AD, in which letters migrate between words, neglect dyslexia, in which letters on one side of the word are omitted or substituted, and surface dyslexia, in which words are read via the sublexical route.We tested 110 children and adults with developmental dyslexia and/or attention deficits, using extensive batteries of reading and attention.For each participant, the existence of dyslexia and the dyslexia type were tested using reading tests that included stimuli sensitive to the various dyslexia types. Attention deficit and its type was established through attention tasks assessing sustained, selective, orienting, and executive attention functioning. Using this procedure,we identified 55 participants who showed a double dissociation between reading and attention: 28 had dyslexia with normal attention and 27 had attention deficits with normal reading.Each dyslexia with suspected attentional basis dissociated from attention:21 individuals with LPD,13 AD,2 neglect dyslexia,and 12 surface dyslexia. Other dyslexia types(vowel dyslexia, phonological dyslexia, visual dyslexia also dissociated from attention deficits.Examination of 55 additional individuals with both a specific dyslexia and a certain attention deficit found no attention function that was consistently linked with any dyslexia type.Specifically, LPD and AD dissociated from selective attention, neglect dyslexia dissociated from orienting, and surface dyslexia dissociated from sustained and executive attention. These results indicate that visuospatial attention deficits do not underlie

  13. Photochemical and antioxidant responses in the leaves of Xerophyta viscosa Baker and Digitaria sanguinalis L. under water deficit.

    Science.gov (United States)

    Ekmekci, Yasemin; Bohms, Andreas; Thomson, Jennifer A; Mundree, Sagadevan G

    2005-01-01

    In this study, photochemical and antioxidant responses of the monocotyledonous resurrection plant Xerophyta viscosa Baker and the crab grass Digitaria sanguinalis L. under water deficit were investigated as a function of time. Water deficit was imposed by withholding irrigation for 21 d. Gas exchange and chlorophyll a fluorescence analyses indicated that the dehydration treatment caused photoinhibition in both species. The reduction in the photosynthesis rate in both species during water deficit probably contributed to the decline in the photochemical efficiency of PSII and electron transport rate. However, the stomatal conductance of both species did not change during treatment whereas the intercellular CO2 pressure increased after 10 d of water deficit treatment. These observations could be related to nonstomatal limitations. The increasing net transpiration rate of both species may have contributed to leaf cooling because of water limitations. Prolonged water deficit resulted in photosynthetic pigment chlorophyll (a + b) and carotenoids content loss in only D. sanguinalis. Both species especially D. sanguinalis had increased the level of anthocyanin after 15 d of treatment, possibly to prevent the damaging effect of photooxidation. The total SOD activity of D. sanguinalis was significantly different from X. viscosa during the treatment. The total peroxidase activity in D. sanguinalis was significantly higher than in X. viscosa. X. viscosa acclimated to water deficit with no ultimate apparent oxidative damage due to endogenous protective mechanisms of resurrection. In case of D. sanguinalis, water deficit induced considerable stress and possibly caused some oxidative damage, despite the upregulation of protection mechanisms.

  14. Low dopamine D5 receptor density in hippocampus in an animal model of attention-deficit/hyperactivity disorder (ADHD)

    DEFF Research Database (Denmark)

    Medin, T; Rinholm, J E; Owe, S G

    2013-01-01

    A state of low dopaminergic activity has been implicated in attention-deficit/hyperactivity disorder (ADHD). The clinical symptoms of ADHD include inattention, impulsivity and hyperactivity, as well as impaired learning; dopaminergic modulation of the functions in the hippocampus is important to ......, indicating a reduced reservoir for insertion of receptors into the plasma membrane. DRs are important for long-term potentiation and long-term depression, hence the deficit may contribute to the learning difficulties in individuals with the diagnosis of ADHD....

  15. Characterization of a Novel Drosophila SERT Mutant: Insights on the Contribution of the Serotonin Neural System to Behaviors.

    Science.gov (United States)

    Hidalgo, Sergio; Molina-Mateo, Daniela; Escobedo, Pía; Zárate, Rafaella V; Fritz, Elsa; Fierro, Angélica; Perez, Edwin G; Iturriaga-Vasquez, Patricio; Reyes-Parada, Miguel; Varas, Rodrigo; Fuenzalida-Uribe, Nicolás; Campusano, Jorge M

    2017-10-18

    A better comprehension on how different molecular components of the serotonergic system contribute to the adequate regulation of behaviors in animals is essential in the interpretation on how they are involved in neuropsychiatric and pathological disorders. It is possible to study these components in "simpler" animal models including the fly Drosophila melanogaster, given that most of the components of the serotonergic system are conserved between vertebrates and invertebrates. Here we decided to advance our understanding on how the serotonin plasma membrane transporter (SERT) contributes to serotonergic neurotransmission and behaviors in Drosophila. In doing this, we characterized for the first time a mutant for Drosophila SERT (dSERT) and additionally used a highly selective serotonin-releasing drug, 4-methylthioamphetamine (4-MTA), whose mechanism of action involves the SERT protein. Our results show that dSERT mutant animals exhibit an increased survival rate in stress conditions, increased basal motor behavior, and decreased levels in an anxiety-related parameter, centrophobism. We also show that 4-MTA increases the negative chemotaxis toward a strong aversive odorant, benzaldehyde. Our neurochemical data suggest that this effect is mediated by dSERT and depends on the 4-MTA-increased release of serotonin in the fly brain. Our in silico data support the idea that these effects are explained by specific interactions between 4-MTA and dSERT. In sum, our neurochemical, in silico, and behavioral analyses demonstrate the critical importance of the serotonergic system and particularly dSERT functioning in modulating several behaviors in Drosophila.

  16. Behavioral and neurochemical effects of alpha lipoic acid associated with omega-3 in tardive dyskinesia induced by chronic haloperidol in rats.

    Science.gov (United States)

    de Araújo, Dayane Pessoa; Camboim, Thaisa Gracielle Martins; Silva, Ana Patrícia Magalhães; Silva, Caio da Fonseca; de Sousa, Rebeca Canuto; Barbosa, Mabson Delâno Alves; Oliveira, Lucidio Clebeson; Cavalcanti, José Rodolfo Lopes de Paiva; Lucena, Eudes Euler de Souza; Guzen, Fausto Pierdoná

    2017-07-01

    Tardive dyskinesia (TD) is characterized by involuntary movements of the lower portion of the face being related to typical antipsychotic therapy. TD is associated with the oxidative imbalance in the basal ganglia. Lipoic acid (LA) and omega-3 (ω-3) are antioxidants acting as enzyme cofactors, regenerating antioxidant enzymes. This study aimed to investigate behavioral and neurochemical effects of supplementation with LA (100 mg/kg) and ω-3 (1 g/kg) in the treatment of TD induced by chronic use of haloperidol (HAL) (1 mg/kg) in rats. Wistar male rats were used, weighing between 180-200 g. The animals were treated chronically (31 days) with LA alone or associated with HAL or ω-3. Motor behavior was assessed by open-field test, the catalepsy test, and evaluation of orofacial dyskinesia. Oxidative stress was accessed by determination of lipid peroxidation and concentration of nitrite. LA and ω-3 alone or associated caused an improvement in motor performance by increasing locomotor activity in the open-field test and decreased the permanence time on the bar in the catalepsy test and decreased the orofacial dyskinesia. LA and ω-3 showed antioxidant effects, decreasing lipid peroxidation and nitrite levels. Thus, the use of LA associated with ω-3 reduced the extrapyramidal effects produced by chronic use of HAL.

  17. Towards a neurochemical profile of the amygdala using short-TE1H magnetic resonance spectroscopy at 3 T.

    Science.gov (United States)

    Schubert, Florian; Kühn, Simone; Gallinat, Jürgen; Mekle, Ralf; Ittermann, Bernd

    2017-05-01

    The amygdala plays a key role in emotional learning and in the processing of emotions. As disturbed amygdala function has been linked to several psychiatric conditions, a knowledge of its biochemistry, especially neurotransmitter levels, is highly desirable. The spin echo full intensity acquired localized (SPECIAL) sequence, together with a transmit/receive coil, was used to perform very short-TE magnetic resonance spectroscopy at 3 T to determine the neurochemical profile in a spectroscopic voxel containing the amygdala in 21 healthy adult subjects. For spectral analysis, advanced data processing was applied in combination with a macromolecule baseline measured in the anterior cingulate for spectral fitting. The concentrations of total N-acetylaspartate, total creatine, total choline, myo-inositol and, for the first time, glutamate were quantified with high reliability (uncertainties far below 10%). For these metabolites, the inter-individual variability, reflected by the relative standard deviations for the cohort studied, varied between 12% (glutamate) and 22% (myo-inositol). Glutamine and glutathione could also be determined, albeit with lower precision. Retest on four subjects showed good reproducibility. The devised method allows the determination of metabolite concentrations in the amygdala voxel, including glutamate, provides an estimation of glutamine and glutathione, and may help in the study of disturbed amygdala metabolism in pathologies such as anxiety disorder, autism and major depression. Copyright © 2017 John Wiley & Sons, Ltd.

  18. Behavioral and Neurochemical Effects of Alpha-Lipoic Acid in the Model of Parkinson’s Disease Induced by Unilateral Stereotaxic Injection of 6-Ohda in Rat

    Directory of Open Access Journals (Sweden)

    Dayane Pessoa de Araújo

    2013-01-01

    Full Text Available This study aimed to investigate behavioral and neurochemical effects of α-lipoic acid (100 mg/kg or 200 mg/kg alone or associated with L-DOPA using an animal model of Parkinson’s disease induced by stereotaxic injection of 6-hydroxydopamine (6-OHDA in rat striatum. Motor behavior was assessed by monitoring body rotations induced by apomorphine, open field test and cylinder test. Oxidative stress was accessed by determination of lipid peroxidation using the TBARS method, concentration of nitrite and evaluation of catalase activity. α-Lipoic acid decreased body rotations induced by apomorphine, as well as caused an improvement in motor performance by increasing locomotor activity in the open field test and use of contralateral paw (in the opposite side of the lesion produced by 6-OHDA at cylinder test. α-lipoic acid showed antioxidant effects, decreasing lipid peroxidation and nitrite levels and interacting with antioxidant system by decreasing of endogenous catalase activity. Therefore, α-lipoic acid prevented the damage induced by 6-OHDA or by chronic use of L-DOPA in dopaminergic neurons, suggesting that α-lipoic could be a new therapeutic target for Parkinson's disease prevention and treatment.

  19. Toward an in Vivo Neurochemical Profile: Quantification of 18 Metabolites in Short-Echo-Time 1H NMR Spectra of the Rat Brain

    Science.gov (United States)

    Pfeuffer, Josef; Tkáč , Ivan; Provencher, Stephen W.; Gruetter, Rolf

    1999-11-01

    Localized in vivo1H NMR spectroscopy was performed with 2-ms echo time in the rat brain at 9.4 T. Frequency domain analysis with LCModel showed that the in vivo spectra can be explained by 18 metabolite model solution spectra and a highly structured background, which was attributed to resonances with fivefold shorter in vivo T1 than metabolites. The high spectral resolution (full width at half maximum approximately 0.025 ppm) and sensitivity (signal-to-noise ratio approximately 45 from a 63-μL volume, 512 scans) was used for the simultaneous measurement of the concentrations of metabolites previously difficult to quantify in 1H spectra. The strongly represented signals of N-acetylaspartate, glutamate, taurine, myo-inositol, creatine, phosphocreatine, glutamine, and lactate were quantified with Cramér-Rao lower bounds below 4%. Choline groups, phosphorylethanolamine, glucose, glutathione, γ-aminobutyric acid, N-acetylaspartylglutamate, and alanine were below 13%, whereas aspartate and scyllo-inositol were below 22%. Intra-assay variation was assessed from a time series of 3-min spectra, and the coefficient of variation was similar to the calculated Cramér-Rao lower bounds. Interassay variation was determined from 31 pooled spectra, and the coefficient of variation for total creatine was 7%. Tissue concentrations were found to be in very good agreement with neurochemical data from the literature.

  20. Imported Case of Lassa Fever in Sweden With Encephalopathy and Sensorineural Hearing Deficit.

    Science.gov (United States)

    Grahn, Anna; Bråve, Andreas; Lagging, Martin; Dotevall, Leif; Ekqvist, David; Hammarström, Helena; Karlberg, Helen; Lagerqvist, Nina; Sansone, Martina; Tegnell, Anders; Ulleryd, Peter; Studahl, Marie

    2016-10-01

    We describe an imported case of Lassa fever with both encephalopathy and bilateral sensorineural hearing deficit. Absence of fever during hospitalization, initially nonspecific symptoms, and onset of hearing deficit in a late stage of disease probably contributed to delayed diagnosis (14 days after admittance to hospital). The pathogenesis of neurological manifestations of Lassa fever is poorly understood and no specific treatment was given. A total of 118 personnel had close contact with the patient, but no secondary cases occurred. This case highlights the importance of considering Lassa fever as a differential diagnosis in patients with recent travel to endemic areas.

  1. Analysis of Budget deficit in Romania during 2000-2013

    OpenAIRE

    Moraru Camelia; Popovici Norina

    2014-01-01

    Worldwide, over time, the years of economic crisis were defined by significant increases in the levels of budget deficits. Discussions on sizing budget deficits, financing, especially the volume of public debt became more intense, both politically and academically. The impact of budget deficit on economic growth is a common theme found in the economic policies adopted. The present paper aims to analyze the evolution of budget deficit and the structural budget deficit in Romania during 2000-20...

  2. What Is the deficit in Phonological Processing Deficits: Auditory Sensitivity, Masking, or Category Formation?

    Science.gov (United States)

    Nittrouer, Susan; Shune, Samantha; Lowenstein, Joanna H.

    2011-01-01

    Although children with language impairments, including those associated with reading, usually demonstrate deficits in phonological processing, there is minimal agreement as to the source of those deficits. This study examined two problems hypothesized to be possible sources: either poor auditory sensitivity to speech-relevant acoustic properties,…

  3. Color perception deficits in co-existing attention-deficit/hyperactivity disorder and chronic tic disorders

    NARCIS (Netherlands)

    Roessner, V.; Banaschewski, T.; Fillmer-Otte, A.; Becker, A.; Albrecht, B.; Uebel, H.; Sergeant, J.A.; Tannock, R.; Rothenberger, A.

    2008-01-01

    Preliminary findings suggest that color perception, particularly of blue-yellow stimuli, is impaired in attention-deficit/hyperactivity disorder (ADHD) as well as in chronic tic disorders (CTD). However, these findings have been not replicated and it is unclear what these deficits mean for the

  4. Color perception deficits in co-existing attention-deficit/hyperactivity disorder and chronic tic disorders.

    Science.gov (United States)

    Roessner, V; Banaschewski, T; Fillmer-Otte, A; Becker, A; Albrecht, B; Uebel, H; Sergeant, J; Tannock, R; Rothenberger, A

    2008-01-01

    Preliminary findings suggest that color perception, particularly of blue-yellow stimuli, is impaired in attention-deficit/hyperactivity disorder (ADHD) as well as in chronic tic disorders (CTD). However, these findings have been not replicated and it is unclear what these deficits mean for the comorbidity of ADHD + CTD. Four groups (ADHD, CTD, ADHD + CTD, controls) of children with similar age, IQ and gender distribution were investigated with the Farnsworth-Munsell 100 Hue Test (FMT) and the Stroop-Color-Word Task using a factorial design. Color perception deficits, as indexed by the FMT, were found for both main factors (ADHD and CTD), but there were no interaction effects. A preponderance of deficits on the blue-yellow compared to the red-green axis was detected for ADHD. In the Stroop task only the 'pure' ADHD group showed impairments in interference control and other parameters of Stroop performance. No significant correlations between any FMT parameter and color naming in the Stroop task were found. Basic color perception deficits in both ADHD and CTD could be found. Beyond that, it could be shown that these deficits are additive in the case of comorbidity (ADHD + CTD). Performance deficits on the Stroop task were present only in the 'pure' ADHD group. Hence, the latter may be compensated in the comorbid group by good prefrontal capabilities of CTD. The influence of color perception deficits on Stroop task performance might be negligible.

  5. The effects of presentation rate and retention interval on memory for items and associations in younger adults: a simulation of older adults' associative memory deficit.

    Science.gov (United States)

    Brubaker, Matthew S; Naveh-Benjamin, Moshe

    2014-01-01

    Older adults show an associative deficit in episodic memory compared to younger adults. Previous research suggests both strategic and automatic binding deficits contribute to older adults' poorer memory performance. Using behavioral manipulations designed to affect strategic and automatic binding of associations, three experiments attempted to simulate an associative deficit in younger adults. In these experiments participants learned face-scene pairs and then were given item and associative recognition memory tests. We manipulated the time allotted at encoding and retrieval to simulate strategic deficits, and the length of the retention interval to simulate automatic deficits. Results indicate that both manipulations separately contribute to a differential decline in associative memory, similar to the one shown by older adults, especially as reflected in the differential increase in false alarm rate in the associative memory test more than in the item memory test. Considerations of possible underlying brain mechanisms are discussed.

  6. Involvement of dopaminergic and cholinergic systems in social isolation-induced deficits in social affiliation and conditional fear memory in mice.

    Science.gov (United States)

    Okada, R; Fujiwara, H; Mizuki, D; Araki, R; Yabe, T; Matsumoto, K

    2015-07-23

    Post-weaning social isolation rearing (SI) in rodents elicits various behavioral abnormalities including attention deficit hyperactivity disorder-like behaviors. In order to obtain a better understanding of SI-induced behavioral abnormalities, we herein investigated the effects of SI on social affiliation and conditioned fear memory as well as the neuronal mechanism(s) underlying these effects. Four-week-old male mice were group-housed (GH) or socially isolated for 2-4 weeks before the experiments. The social affiliation test and fear memory conditioning were conducted at the age of 6 and 7 weeks, respectively. SI mice were systemically administered saline or test drugs 30 min before the social affiliation test and fear memory conditioning. Contextual and auditory fear memories were elucidated 1 and 4 days after fear conditioning. Social affiliation and contextual and auditory fear memories were weaker in SI mice than in GH mice. Methylphenidate (MPH), an inhibitor for dopamine transporters, ameliorated the SI-induced social affiliation deficit and the effect was attenuated by SCH23390, a D1 receptor antagonist, but not by sulpiride, a D2 receptor antagonist. On the other hand, tacrine, an acetylcholinesterase inhibitor, had no effect on this deficit. In contrast, tacrine improved SI-induced deficits in fear memories in a manner that was reversed by the muscarinic receptor antagonist scopolamine, while MPH had no effect on memory deficits. Neurochemical studies revealed that SI down-regulated the expression levels of the phosphorylated forms of neuro-signaling proteins, calmodulin-dependent kinase II (p-CaMKII), and cyclic AMP-responsive element binding protein (p-CREB), as well as early growth response protein-1 (Egr-1) in the hippocampus. The administration of MPH or tacrine before fear conditioning had no effect on the levels of the phosphorylated forms of the neuro-signaling proteins elucidated following completion of the auditory fear memory test; however

  7. Test Differences in Diagnosing Reading Comprehension Deficits

    Science.gov (United States)

    Keenan, Janice M.; Meenan, Chelsea E.

    2012-01-01

    We examined the implications of test differences for defining and diagnosing comprehension deficits using reading comprehension tests. We had 995 children complete the Gray Oral Reading Test-3, the Qualitative Reading Inventory-3, the Woodcock-Johnson Passage Comprehension-3, and the Peabody Individual Achievement Test, and compared which children were identified by each test as being in the lowest 10%. Although a child who performs so poorly might be expected to do poorly on all tests, we found that the average overlap between tests in diagnosing comprehension difficulties was only 43%. Consistency in diagnosis was greater for younger children, when comprehension deficits are due to weaker decoding skills, than for older children. Inconsistencies between tests were just as evident when identifying the top performers. The different children identified as having a comprehension deficit by each test were compared on four profile variables - word decoding skill, IQ, ADHD symptoms, and working memory skill – to understand the nature of the different deficits assessed by each test. Theoretical and practical implications of these test differences in defining and diagnosing comprehension deficits are discussed. PMID:22442251

  8. Social-Cognitive Deficits in Schizophrenia.

    Science.gov (United States)

    Mier, Daniela; Kirsch, Peter

    Patients with schizophrenia not only suffer from prototypical psychotic symptoms such as delusions and hallucinations and from cognitive deficits, but also from tremendous deficits in social functioning. However, little is known about the interplay between the cognitive and the social-cognitive deficits in schizophrenia. Our chapter gives an overview on behavioral, as well as functional imaging studies on social cognition in schizophrenia. Main findings on cognitive and motivational deficits in schizophrenia are reviewed and introduced within the context of the dopamine hypothesis of schizophrenia. The reviewed findings suggest that disturbed "social brain" functioning in schizophrenia, depending on the specific context, can either lead to a neglect of the emotions and intentions of others or to the false attribution of these emotions and intentions in an emotionally neutral social content. We integrate these findings with the current knowledge about aberrant dopaminergic firing in schizophrenia by presenting a comprehensive model explaining core symptoms of the disorder. The main implication of the presented model is that neither cognitive-motivational, nor social-cognitive deficits alone cause schizophrenia symptoms, but that symptoms only emerge by the interplay of disturbed social brain functioning with aberrant dopaminergic firing.

  9. Reducing attention deficits after stroke using attention process training: a randomized controlled trial.

    Science.gov (United States)

    Barker-Collo, Suzanne L; Feigin, Valery L; Lawes, Carlene M M; Parag, Varsha; Senior, Hugh; Rodgers, Anthony

    2009-10-01

    Impaired attention contributes to poor stroke outcomes. Attention process training (APT) reduces attention deficits after traumatic brain injury. There was no evidence for effectiveness of APT in stroke patients. This trial evaluated effectiveness of APT in improving attention and broader outcomes in stroke survivors 6 months after stroke. Participants in this prospective, single-blinded, randomized, clinical trial were 78 incident stroke survivors admitted over 18 months and identified via neuropsychological assessment as having attention deficit. Participants were randomly allocated to standard care plus up to 30 hours of APT or standard care alone. Both groups were impaired (z attention at baseline, with the exception of Paced Auditory Serial Addition Test, which was below average (z Attention Quotient. APT resulted in a significantly greater (Pattention and broader outcomes were not significant. APT is a viable and effective means of improving attention deficits after incident stroke.

  10. Fear-learning deficits in subjects with fibromyalgia syndrome?

    Science.gov (United States)

    Jenewein, J.; Moergeli, H.; Sprott, H.; Honegger, D.; Brunner, L.; Ettlin, D.; Grillon, C.; Bloch, K.; Brügger, M.; Schwegler, K.; Schumacher, S.; Hasler, G.

    2014-01-01

    Background Fibromyalgia syndrome (FMS) is frequently associated with psychiatric conditions, particularly anxiety. Deficits in contingency learning during fear conditioning have been hypothesized to increase anxiety and, consequently, pain sensation in susceptible individuals. The goal of this study was to examine the relationship between contingency learning and pain experience in subjects with FMS and rheumatoid arthritis (RA). Methods Fourteen female FMS subjects, 14 age-matched female RA subjects and 14 age-matched female healthy controls (HCs) were included in a fear-conditioning experiment. The conditioned stimulus (CS) consisted of visual signs, the unconditioned stimulus (US) of thermal stimuli. CS− predicted low-temperature exposure (US), while CS+ was followed by low or high temperature. Results In the FMS group, only 50% of the subjects were aware of the US–CS contingency, whereas 86% of the RA subjects and all of the HCs were aware of the contingency. CS+ induced more anxiety than CS− in RA subjects and HCs. As expected, low-temperature exposure was experienced as less painful after CS− than after CS+ in these subjects. FMS subjects did not show such adaptive conditioning. The effects of the type of CS on heart rate changes were significant in the HCs and the aware FMS subjects, but not in the unaware FMS subjects. Conclusions Contingency learning deficits represent a potentially promising and specific, but largely unstudied, psychopathological factor in FMS. Deficits in contingency learning may increase anxiety and, consequently, pain sensation. These findings have the potential to contribute to the development of novel therapeutic approaches for FMS. PMID:23468076

  11. Deficits in striatal dopamine release in cannabis dependence.

    Science.gov (United States)

    van de Giessen, E; Weinstein, J J; Cassidy, C M; Haney, M; Dong, Z; Ghazzaoui, R; Ojeil, N; Kegeles, L S; Xu, X; Vadhan, N P; Volkow, N D; Slifstein, M; Abi-Dargham, A

    2017-01-01

    Most drugs of abuse lead to a general blunting of dopamine release in the chronic phase of dependence, which contributes to poor outcome. To test whether cannabis dependence is associated with a similar dopaminergic deficit, we examined striatal and extrastriatal dopamine release in severely cannabis-dependent participants (CD), free of any comorbid conditions, including nicotine use. Eleven CD and 12 healthy controls (HC) completed two positron emission tomography scans with [11C]-(+)-PHNO, before and after oral administration of d-amphetamine. CD stayed inpatient for 5-7 days prior to the scans to standardize abstinence. Magnetic resonance spectroscopy (MRS) measures of glutamate in the striatum and hippocampus were obtained in the same subjects. Percent change in [11C]-(+)-PHNO-binding potential (ΔBPND) was compared between groups and correlations with MRS glutamate, subclinical psychopathological and neurocognitive parameters were examined. CD had significantly lower ΔBPND in the striatum (P=0.002, effect size (ES)=1.48), including the associative striatum (P=0.003, ES=1.39), sensorimotor striatum (P=0.003, ES=1.41) and the pallidus (P=0.012, ES=1.16). Lower dopamine release in the associative striatum correlated with inattention and negative symptoms in CD, and with poorer working memory and probabilistic category learning performance in both CD and HC. No relationships to MRS glutamate and amphetamine-induced subclinical positive symptoms were detected. In conclusion, this study provides evidence that severe cannabis dependence-without the confounds of any comorbidity-is associated with a deficit in striatal dopamine release. This deficit extends to other extrastriatal areas and predicts subclinical psychopathology.

  12. Neuropsychological deficits in patients with Lyme borreliosis

    Directory of Open Access Journals (Sweden)

    Katja Pruša

    2001-09-01

    Full Text Available Slovenia is an endemic area for Lyme borreliosis, a disease that affects many organic systems. Decline in cognitive abilities and emotional changes can appear in acute and chronic stage of the disease beside somatic difficulties. Early antibiotic therapy is of great importance in recovery. Attention and concentration deficits, memory deficits, impaired executive functioning, depression and other symptoms reduce work efficiency and life quality of people with Lyme borreliosis. Neuropsychological deficits can be explained with central nervous system impairment and partly also with reactive psychological factors. On account of symptomatic complexity, broad differential diagnostic and unreliable diagnostic technology neuropsychological evaluation can help to correctly diagnose and accurately treat this disease, and thus to enable appropriate cognitive rehabilitation and psychotherapeutic assistance.

  13. Neurocognitive Deficits in Borderline Personality Disorder

    DEFF Research Database (Denmark)

    Thomsen, Marianne Skovgaard; Ruocco, Anthony C; Carcone, Dean

    2017-01-01

    The present study evaluates the severity of neurocognitive deficits and assesses their relations with self-reported childhood trauma and dimensions of personality psychopathology in 45 outpatients with borderline personality disorder (BPD) matched to 56 non-psychiatric controls. Participants...... completed a comprehensive battery of neurocognitive tests, a retrospective questionnaire on early life trauma and a dimensional measure of personality psychopathology. Patients with BPD primarily showed deficits in verbal comprehension, sustained visual attention, working memory and processing speed....... Comorbid posttraumatic stress disorder (PTSD) and an elevated childhood history of physical trauma were each accompanied by more severe neurocognitive deficits. There were no statistically significant associations between neurocognitive function and dimensions of personality psychopathology. These results...

  14. Working memory deficits of reading disabled children.

    Science.gov (United States)

    de Jong, P F

    1998-08-01

    Aims of the study were to investigate the specificity of reading disabled childrens deficits in working memory capacity and to pursue whether their deficits could be accounted for by deficient processing or impairments in verbal short-term storage capacity. A group of 10-year-old reading disabled children was compared with two groups of normal reading children, matched for chronological age and reading age, respectively. Measures for working memory capacity, short-term capacity and processing speed related to the language and to the numerical domain were administered. Results indicated that reading disabled children performed worse on all measures of working memory capacity, irrespective of the domain which these measures reflected. Their poorer performance could neither be explained by inefficient processing nor to their deficits in verbal short-term storage capacity. Reading disabled children seem to have a general lack of capacity for the concurrent processing and storage of verbal information. Copyright 1998 Academic Press.

  15. Plasma membrane ordering agent pluronic F-68 (PF-68) reduces neurotransmitter uptake and release and produces learning and memory deficits in rats

    Science.gov (United States)

    Clarke, M. S.; Prendergast, M. A.; Terry, A. V. Jr

    1999-01-01

    A substantial body of evidence indicates that aged-related changes in the fluidity and lipid composition of the plasma membrane contribute to cellular dysfunction in humans and other mammalian species. In the CNS, reductions in neuronal plasma membrane order (PMO) (i.e., increased plasma membrane fluidity) have been attributed to age as well as the presence of the beta-amyloid peptide-25-35, known to play an important role in the neuropathology of Alzheimer's disease (AD). These PMO increases may influence neurotransmitter synthesis, receptor binding, and second messenger systems as well as signal transduction pathways. The effects of neuronal PMO on learning and memory processes have not been adequately investigated, however. Based on the hypothesis that an increase in PMO may alter a number of aspects of synaptic transmission, we investigated several neurochemical and behavioral effects of the membrane ordering agent, PF-68. In cell culture, PF-68 (nmoles/mg SDS extractable protein) reduced [3H]norepinephrine (NE) uptake into differentiated PC-12 cells as well as reduced nicotine stimulated [3H]NE release. The compound (800-2400 microg/kg, i.p., resulting in nmoles/mg SDS extractable protein in the brain) decreased step-through latencies and increased the frequencies of crossing into the unsafe side of the chamber in inhibitory avoidance training. In the Morris water maze, PF-68 increased the latencies and swim distances required to locate a hidden platform and reduced the time spent and distance swam in the previous target quadrant during transfer (probe) trials. PF-68 did not impair performance of a well-learned working memory task, the rat delayed stimulus discrimination task (DSDT), however. Studies with 14C-labeled PF-68 indicated that significant (pmoles/mg wet tissue) levels of the compound entered the brain from peripheral (i.p.) injection. No PF-68 related changes were observed in swim speeds or in visual acuity tests in water maze experiments, rotorod

  16. Living in a family with a child with attention deficit hyperactivity disorder: a phenomenographic study.

    Science.gov (United States)

    Moen, Øyfrid Larsen; Hall-Lord, Marie Louise; Hedelin, Birgitta

    2014-11-01

    To describe experiences of everyday life in families with a child with attention deficit hyperactivity disorder. Attention deficit hyperactivity disorder is a highly prevalent, clinically heterogeneous disorder characterised by behavioural symptoms of inattention, hyperactivity and impulsivity that creates impairments for the child and affects the family life. The impairments vary with age and context, and the same symptoms do not necessarily have the same effects in different contexts and persons. A qualitative design with a phenomenographic approach. Family members, mothers, fathers, siblings and children with attention deficit hyperactivity disorder (n = 17) were interviewed individually. The findings include two descriptive categories 'safeguarding a functioning family' and 'fighting for acceptance and inclusion'. To create a stable and structured family life to avoid conflicts within the family and manage their daily life were crucial. The child with attention deficit hyperactivity disorder and their parents developed special skills and strategies to live with attention deficit hyperactivity disorder in the family sphere and the social context. To apply for help before the problems in the family become too severe and to share responsibility with professionals, who have competence, to meet the families in their worries were stressed. The striving in the family strengthened the companionship in the families, and they conceived growth. This study contributes to knowledge of the parents, siblings and children with attention deficit hyperactivity disorder experiences of everyday life with a child with attention deficit hyperactivity disorder. All family members need support before their problems become too severe. There is a need of family-focused approach with a dialogue with family members to share the view of their situation and identify their individual resources and needs. Nurses should help these families with family supervision.

  17. Gestantes/puérperas com hiv/aids: conhecendo os déficits e os fatores que contribuem no engajamento para o autocuidado Gestantes/puérperas con el vih/sida: conociendo los déficits y los factores que contribuyen para el compromiso con el autocuidado Pregnant women/mothers with newborns with hiv/aids: understanding the deficits and factors that contribute to engaging in self-care

    Directory of Open Access Journals (Sweden)

    Lígia Maria Scherer

    2009-06-01

    ón social. Las gestantes/puérperas conviven con factores que contribuyen para el compromiso con el autocuidado, así como con factores que lo dificultan. Pero a pesar de las dificultades, ellas han conseguido sobrevivir al aislamiento y al prejuicio gracias al apoyo familiar y a la ayuda del equipo de salud, especialmente de las enfermeras.The objective of this qualitative, descriptive, exploratory study is to better understand the deficits of self-care among pregnant women/ mothers with newborns with HIV/AIDS and the factors that influence engagement with self-care. The study was carried out with ten pregnant women/mothers of newborns with HIV who use the Specialized Service for STD/Aids in Rio Grande do Sul, Brazil. The data was collected through a focus group and individual interviews, using a semi-structured script. After analyzing the data through content analysis, the following results were reached: the pregnant women/ mothers of newborns with HIV present deficits to self-care related to nutrition and feeding, water ingestion, sleep and rest, sexual life, leisure and recreation, and social interaction. They live so continuously with factors that contribute to engaging in self-care as factors that make this process difficult. Even with these difficulties, the pregnant women/ mothers of newborns have been able to survive into the isolation, the prejudice, receiving a support from their families and from the health care team, especially from nurses.

  18. Growth deficits in cystic fibrosis mice begin in utero prior to IGF-1 reduction.

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    Rebecca Darrah

    Full Text Available Growth deficits are common in cystic fibrosis (CF, but their cause is complex, with contributions from exocrine pancreatic insufficiency, pulmonary complications, gastrointestinal obstructions, and endocrine abnormalities. The CF mouse model displays similar growth impairment despite exocrine pancreatic function and in the absence of chronic pulmonary infection. The high incidence of intestinal obstruction in the CF mouse has been suggested to significantly contribute to the observed growth deficits. Previous studies by our group have shown that restoration of the cystic fibrosis transmembrane conductance regulator (CFTR in the intestinal epithelium prevents intestinal obstruction but does not improve growth. In this study, we further investigate growth deficits in CF and gut-corrected CF mice by assessing insulin-like growth factor 1 (IGF-1. IGF-1 levels were significantly decreased in CF and gut-corrected CF adult mice compared to wildtype littermates and were highly correlated with weight. Interestingly, perinatal IGF-1 levels were not significantly different between CF and wildtype littermates, even though growth deficits in CF mice could be detected late in gestation. Since CFTR has been suggested to play a role in water and nutrient exchange in the placenta through its interaction with aquaporins, we analyzed placental aquaporin expression in late-gestation CF and control littermates. While significant differences were observed in Aquaporin 9 expression in CF placentas in late gestation, there was no evidence of placental fluid exchange differences between CF and control littermates. The results from this study indicate that decreased IGF-1 levels are highly correlated with growth in CF mice, independent of CF intestinal obstruction. However, the perinatal growth deficits that are observed in CF mice are not due to decreased IGF-1 levels or differences in placenta-mediated fluid exchange. Further investigation is necessary to understand

  19. Hypothesis-Driven Treatment of Naming Deficits.

    Science.gov (United States)

    Robinson, K M; Grossman, M

    1997-01-01

    This article proposes to use information processing models of cognition to guide behaviorally based treatments of language deficits, specifically, single-word object naming. Our approach is illustrated with a clinical case of a transcortical sensory aphasic. Clinical neuropsychological and functional imaging data demonstrate that the components comprising the information processing network that underpins naming can be mapped onto a cerebral neural network in the neurologically intact and that reorganization of function seen in transcortical sensory aphasia can demonstrate plasticity in this neural network. The observed balance of impaired and preserved clinical and physiological components in reorganizing neural networks such as this can be used to design treatment strategies to alleviate naming deficits.

  20. The history of attention deficit hyperactivity disorder

    Science.gov (United States)

    Reichl, Susanne; Lange, Katharina M.; Tucha, Lara; Tucha, Oliver

    2010-01-01

    The contemporary concept of attention deficit hyperactivity disorder (ADHD) as defined in the DSM-IV-TR (American Psychiatric Association 2000) is relatively new. Excessive hyperactive, inattentive, and impulsive children have been described in the literature since the nineteenth century. Some of the early depictions and etiological theories of hyperactivity were similar to current descriptions of ADHD. Detailed studies of the behavior of hyperactive children and increasing knowledge of brain function have changed the concepts of the fundamental behavioral and neuropathological deficits underlying the disorder. This article presents an overview of the conceptual history of modern-day ADHD. PMID:21258430

  1. Deficit of entropy modulation of the EEG in schizophrenia associated to cognitive performance and symptoms. A replication study.

    Science.gov (United States)

    Molina, Vicente; Bachiller, Alejandro; Gomez-Pilar, Javier; Lubeiro, Alba; Hornero, Roberto; Cea-Cañas, Benjamín; Valcárcel, César; Haidar, Mahmoun-Karim; Poza, Jesús

    2017-09-05

    Spectral entropy (SE) is a measurement from information theory field that provides an estimation of EEG regularity and may be useful as a summary of its spectral properties. Previous studies using small samples reported a deficit of EEG entropy modulation in schizophrenia during cognitive activity. The present study is aimed at replicating this finding in a larger sample, to explore its cognitive and clinical correlates and to discard antipsychotic treatment as the main source of that deficit. We included 64 schizophrenia patients (21 first episodes, FE) and 65 healthy controls. We computed SE during performance of an odd-ball paradigm, at the windows prior (-300 to 0ms) and following (150 to 450ms) stimulus presentation. Modulation of SE was defined as the difference between post- and pre-stimulus windows. In comparison to controls, patients showed a deficit of SE modulation over frontal and central regions, also shown by FE patients. Baseline SE did not differ between patients and controls. Modulation deficit was directly associated with cognitive deficits and negative symptoms, and inversely with positive symptoms. SE modulation was not related to antipsychotic doses. Patients also showed a smaller change of median frequency (i.e., smaller slowing of oscillatory activity) of the EEG from pre- to post-stimulus windows. These results support that a deficit of fast modulation contributes to cognitive deficits and symptoms in schizophrenia patients. Copyright © 2017. Published by Elsevier B.V.

  2. Serum ApoB levels in depressive patients: associated with cognitive deficits.

    Science.gov (United States)

    Hui, Li; Han, Mei; Du, Xiang Dong; Zhang, Bao Hua; He, Shu Chang; Shao, Tian Nan; Yin, Guang Zhong

    2017-01-05

    Cognitive deficits have been regarded as one of the most significant clinical symptoms of depressive disorder. Accumulating evidence has shown that apolipoprotein B (ApoB) levels, which are responsible for inducing neurodegeneration, may be involved in cognitive deficits. This study examines cognitive deficits, and the correlation of serum ApoB levels with cognitive deficits of depressive disorder. 90 depressive patients and 90 healthy controls with matched age and gender were recruited. Cognition was assessed using the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS). Serum ApoB levels in depressive patients were measured by immunoturbidimetric method. Our results showed that depressive patients had lower scores of cognition including RBANS total score and subscales of language and delayed memory (all, p cognitive functions also passed Bonferroni corrections. Serum ApoB levels were negatively correlated with delayed memory score in depressive patients (r = -0.30, p = 0.01). Furthermore, stepwise multivariate regression analysis indicated that serum ApoB levels independently contributed to delayed memory in depressive patients (t = -2.68, p = 0.01). Our findings support that serum ApoB levels may be involved in delayed memory decline in depressive patients. Depressive patients also experience greater cognitive deficits, especially in delayed memory and language than healthy controls.

  3. A Mitochondrion-Targeted Antioxidant Ameliorates Isoflurane-Induced Cognitive Deficits in Aging Mice.

    Science.gov (United States)

    Wu, Jing; Li, Huihui; Sun, Xiaoru; Zhang, Hui; Hao, Shuangying; Ji, Muhuo; Yang, Jianjun; Li, Kuanyu

    2015-01-01

    Isoflurane possesses neurotoxicity and can induce cognitive deficits, particularly in aging mammals. Mitochondrial reactive oxygen species (mtROS) have been linked to the early pathogenesis of this disorder. However, the role of mtROS remains to be evaluated due to a lack of targeted method to treat mtROS. Here, we determined in aging mice the effects of the mitochondrion-targeted antioxidant SS-31, on cognitive deficits induced by isoflurane, a general inhalation anesthetic. We further investigated the possible mechanisms underlying the effects of SS-31 on hippocampal neuro-inflammation and apoptosis. The results showed that isoflurane induced hippocampus-dependent memory deficit, which was associated with mitochondrial dysfunction including reduced ATP contents, increased ROS levels, and mitochondrial swelling. Treatment with SS-31 significantly ameliorated isoflurane-induced cognitive deficits through the improvement of mitochondrial integrity and function. Mechanistically, SS-31 treatment suppressed pro-inflammatory responses by decreasing the levels of NF-κB, NLRP3, caspase 1, IL-1β, and TNF-α; and inhibited the apoptotic pathway by decreasing the Bax/Bcl-2 ratio, reducing the release of cytochrome C, and blocking the cleavage of caspase 3. Our results indicate that isoflurane-induced cognitive deficits may be attenuated by mitochondrion-targeted antioxidants, such as SS-31. Therefore, SS-31 may have therapeutic potentials in preventing injuries from oxidative stresses that contribute to anesthetic-induced neurotoxicity.

  4. Investigating consummatory and anticipatory pleasure across motivation deficits in schizophrenia and healthy controls.

    Science.gov (United States)

    Da Silva, Susana; Saperia, Sarah; Siddiqui, Ishraq; Fervaha, Gagan; Agid, Ofer; Daskalakis, Z Jeff; Ravindran, Arun; Voineskos, Aristotle N; Zakzanis, Konstantine K; Remington, Gary; Foussias, George

    2017-08-01

    Anhedonia has traditionally been considered a characteristic feature of schizophrenia, but the true nature of this deficit remains elusive. This study sought to investigate consummatory and anticipatory pleasure as it relates to motivation deficits. Eighty-four outpatients with schizophrenia and 81 healthy controls were administered the Temporal Experience of Pleasure Scale (TEPS), as well as a battery of clinical and cognitive assessments. Multivariate analyses of variance were used to examine the experience of pleasure as a function of diagnosis, and across levels of motivation deficits (i.e. low vs. moderate. vs. high) in schizophrenia. Hierarchical regression analyses were also conducted to evaluate the predictive value of amotivation in relation to the TEPS. There were no significant differences between schizophrenia and healthy control groups for either consummatory or anticipatory pleasure. Within the schizophrenia patients, only those with high levels of amotivation were significantly impaired in consummatory and anticipatory pleasure compared to low and moderate groups, and compared to healthy controls. Further, our results revealed that amotivation significantly predicts both consummatory and anticipatory pleasure, with no independent contribution of group. Utilizing study samples with a wide range of motivation deficits and incorporating objective paradigms may provide a more comprehensive understanding of hedonic deficits. Copyright © 2017 Elsevier Ireland Ltd. All rights reserved.

  5. A Mitochondrion-Targeted Antioxidant Ameliorates Isoflurane-Induced Cognitive Deficits in Aging Mice.

    Directory of Open Access Journals (Sweden)

    Jing Wu

    Full Text Available Isoflurane possesses neurotoxicity and can induce cognitive deficits, particularly in aging mammals. Mitochondrial reactive oxygen species (mtROS have been linked to the early pathogenesis of this disorder. However, the role of mtROS remains to be evaluated due to a lack of targeted method to treat mtROS. Here, we determined in aging mice the effects of the mitochondrion-targeted antioxidant SS-31, on cognitive deficits induced by isoflurane, a general inhalation anesthetic. We further investigated the possible mechanisms underlying the effects of SS-31 on hippocampal neuro-inflammation and apoptosis. The results showed that isoflurane induced hippocampus-dependent memory deficit, which was associated with mitochondrial dysfunction including reduced ATP contents, increased ROS levels, and mitochondrial swelling. Treatment with SS-31 significantly ameliorated isoflurane-induced cognitive deficits through the improvement of mitochondrial integrity and function. Mechanistically, SS-31 treatment suppressed pro-inflammatory responses by decreasing the levels of NF-κB, NLRP3, caspase 1, IL-1β, and TNF-α; and inhibited the apoptotic pathway by decreasing the Bax/Bcl-2 ratio, reducing the release of cytochrome C, and blocking the cleavage of caspase 3. Our results indicate that isoflurane-induced cognitive deficits may be attenuated by mitochondrion-targeted antioxidants, such as SS-31. Therefore, SS-31 may have therapeutic potentials in preventing injuries from oxidative stresses that contribute to anesthetic-induced neurotoxicity.

  6. Aging-associated excess formaldehyde leads to spatial memory deficits

    Science.gov (United States)

    Tong, Zhiqian; Han, Chanshuai; Luo, Wenhong; Li, Hui; Luo, Hongjun; Qiang, Min; Su, Tao; Wu, Beibei; Liu, Ying; Yang, Xu; Wan, You; Cui, Dehua; He, Rongqiao

    2013-01-01

    Recent studies show that formaldehyde participates in DNA demethylation/methylation cycle. Emerging evidence identifies that neuronal activity induces global DNA demethylation and re-methylation; and DNA methylation is a critical step for memory formation. These data suggest that endogenous formaldehyde may intrinsically link learning-responsive DNA methylation status and memory formation. Here, we report that during spatial memory formation process, spatial training induces an initial global DNA demethylation and subsequent re-methylation associated with hippocampal formaldehyde elevation then decline to baseline level in Sprague Dawley rats. Scavenging this elevated formaldehyde by formaldehyde-degrading enzyme (FDH), or enhancing DNA demethylation by a DNA demethylating agent, both led to spatial memory deficits by blocking DNA re-methylation in rats. Furthermore, we found that the normal adult rats intrahippocampally injected with excess formaldehyde can imitate the aged-related spatial memory deficits and global DNA methylation decline. These findings indicate that aging-associated excess formaldheyde contributes to cognitive decline during aging. PMID:23657727

  7. Crowding deficits in the visual periphery of schizophrenia patients.

    Directory of Open Access Journals (Sweden)

    Rainer Kraehenmann

    Full Text Available Accumulating evidence suggests that basic visual information processing is impaired in schizophrenia. However, deficits in peripheral vision remain largely unexplored. Here we hypothesized that sensory processing of information in the visual periphery would be impaired in schizophrenia patients and, as a result, crowding - the breakdown in target recognition that occurs in cluttered visual environments - would be stronger. Therefore, we assessed visual crowding in the peripheral vision of schizophrenia patients and healthy controls. Subjects were asked to identify a target letter that was surrounded by distracter letters of similar appearance. Targets and distracters were displayed at 8° and 10° of visual angle from the fixation point (eccentricity, and target-distracter spacing was 2°, 3°, 4°, 5°, 6°, 7° or 8° of visual angle. Eccentricity and target-distracter spacing were randomly varied. Accuracy was defined as the proportion of correctly identified targets. Critical spacing was defined as the spacing at which target identification accuracy began to deteriorate, and was assessed at viewing eccentricities of 8° and 10°. Schizophrenia patients were less accurate and showed a larger critical spacing than healthy individuals. These results indicate that crowding is stronger and sensory processing of information in the visual periphery is impaired in schizophrenia. This is in line with previous reports of preferential magnocellular dysfunction in schizophrenia. Thus, deficits in peripheral vision may account for perceptual alterations and contribute to cognitive dysfunction in schizophrenia.

  8. Social cognition and neurocognitive deficits in first-episode schizophrenia.

    Science.gov (United States)

    Bliksted, Vibeke; Fagerlund, Birgitte; Weed, Ethan; Frith, Chris; Videbech, Poul

    2014-03-01

    Recent research has shown a significant impact of social cognitive domains on real world functioning and prognosis in schizophrenia. However, the correlations between specific aspects of social cognition, neurocognition, IQ and clinical symptoms remain unclear in first-episode schizophrenia. Researchers have speculated about social cognitive subgroups since patients with schizophrenia appear to be a very heterogeneous group. Patients with a recent diagnosis of first-episode schizophrenia were tested regarding theory of mind, social perception, neurocognition, IQ, and clinical symptoms. Data from 36 first-episode schizophrenia patients and 36 one to one matched healthy controls were analysed. Principal component analysis in the patient group was used to examine the variance contributed by different aspects of social cognition, neurocognition, and clinical symptoms. Complex aspects of social cognition explained 24% of the variance in the patient group. The other principal components consisted mainly of aspects of simple perception of theory of mind. Neurocognition and clinical symptoms only explained a minor proportion of the variance in the patient group. The results imply that social cognitive deficits in first-episode schizophrenia come in two distinct versions where one is a complex, cognitive demanding form linked with IQ. The other version is related to simpler forms of social cognition and independent of IQ. These two forms are comparable to the implicit and explicit mentalising discussed in the developmental literature. The two forms of social cognitive deficits are likely to require quite different social cognitive interventions. Copyright © 2014 Elsevier B.V. All rights reserved.

  9. Deficits in reflexive covert attention following cerebellar injury.

    Directory of Open Access Journals (Sweden)

    Christopher eStriemer

    2015-08-01

    Full Text Available Traditionally the cerebellum has been known for its important role in coordinating motor output. Over the past fifteen years numerous studies have indicated that the cerebellum plays a role in a variety of cognitive functions including working memory, language, perceptual functions, and emotion. In addition, recent work suggests that regions of the cerebellum involved in eye movements also play a role in controlling covert visual attention. Here we investigated whether regions of the cerebellum that are not strictly tied to the control of eye movements might also contribute to covert attention. To address this question we examined the effects of circumscribed cerebellar lesions on reflexive covert attention in a group of patients (n=11 without any gross motor or oculomotor deficits, and compared their performance to a group of age-matched controls (n=11. Results indicated that the traditional RT advantage for validly cued targets was significantly smaller at the shortest (50ms SOA for cerebellar patients compared to controls. Critically, a lesion overlap analysis indicated that this deficit in the rapid deployment of attention was linked to damage in Crus I and Crus II of the lateral cerebellum. Importantly, both cerebellar regions have connections to non-motor regions of the prefrontal and posterior parietal cortices – regions important for controlling visuospatial attention. Together, these data provide converging evidence that both lateral and midline regions of the cerebellum play an important role in the control of reflexive covert visual attention.

  10. Deficits in reflexive covert attention following cerebellar injury.

    Science.gov (United States)

    Striemer, Christopher L; Cantelmi, David; Cusimano, Michael D; Danckert, James A; Schweizer, Tom A

    2015-01-01

    Traditionally the cerebellum has been known for its important role in coordinating motor output. Over the past 15 years numerous studies have indicated that the cerebellum plays a role in a variety of cognitive functions including working memory, language, perceptual functions, and emotion. In addition, recent work suggests that regions of the cerebellum involved in eye movements also play a role in controlling covert visual attention. Here we investigated whether regions of the cerebellum that are not strictly tied to the control of eye movements might also contribute to covert attention. To address this question we examined the effects of circumscribed cerebellar lesions on reflexive covert attention in a group of patients (n = 11) without any gross motor or oculomotor deficits, and compared their performance to a group of age-matched controls (n = 11). Results indicated that the traditional RT advantage for validly cued targets was significantly smaller at the shortest (50 ms) SOA for cerebellar patients compared to controls. Critically, a lesion overlap analysis indicated that this deficit in the rapid deployment of attention was linked to damage in Crus I and Crus II of the lateral cerebellum. Importantly, both cerebellar regions have connections to non-motor regions of the prefrontal and posterior parietal cortices-regions important for controlling visuospatial attention. Together, these data provide converging evidence that both lateral and midline regions of the cerebellum play an important role in the control of reflexive covert visual attention.

  11. Neurochemical correlates of accumbal dopamine D2 and amygdaloid 5-HT 1B receptor densities on observational learning of aggression.

    Science.gov (United States)

    Suzuki, Hideo; Lucas, Louis R

    2015-06-01

    Social learning theory postulates that individuals learn to engage in aggressive behavior through observing an aggressive social model. Prior studies have shown that repeatedly observing aggression, also called "chronic passive exposure to aggression," changes accumbal dopamine D2 receptor (D2R) and amygdaloid 5-HT1B receptor (5-HT1BR) densities in observers. But, the association between these outcomes remains unknown. Thus, in our study, we used a rat paradigm to comprehensively examine the linkage between aggression, D2R density in the nucleus accumbens core (AcbC) and shell (AcbSh), and 5-HT1BR density in the medial (MeA), basomedial (BMA), and basolateral (BLA) amygdala following chronic passive exposure to aggression. Male Sprague-Dawley rats (N = 72) were passively exposed to either aggression or nonaggression acutely (1 day) or chronically (23 days). When observer rats were exposed to aggression chronically, they showed increased aggressive behavior and reduced D2R density in bilateral AcbSh. On the other hand, exposure to aggression, regardless of exposure length, increased the 5-HT1BR density in bilateral BLA. Finally, low D2R in the AcbSh significantly interacted with high 5-HT1BR density in the BLA to predict high levels of aggression in observer rats. Our results advance our understanding of the neurobiological mechanisms in the observational learning of aggression, highlighting that dopamine-serotonin interaction, or AcbSh-BLA interaction, may contribute to a risk factor for aggression in observers who chronically witness aggressive interactions.

  12. Neurochemical Correlates of Accumbal Dopamine D2 and Amygdaloid 5-HT1B Receptor Densities on Observational Learning of Aggression

    Science.gov (United States)

    Suzuki, Hideo; Lucas, Louis R.

    2015-01-01

    Social learning theory postulates that individuals learn to engage in aggressive behavior through observing an aggressive social model. Prior studies have shown that repeatedly observing aggression, also called “chronic passive exposure to aggression,” changes accumbal dopamine D2 receptor (D2R) and amygdaloid 5-HT1B receptor (5-HT1BR) densities in observers. But, the association between these outcomes remains unknown. Thus, our study used a rat paradigm to comprehensively examine the linkage between aggression, D2R density in the nucleus accumbens core (AcbC) and shell (AcbSh), and 5-HT1BR density in the medial (MeA), basomedial (BMA), and basolateral (BLA) amygdala following chronic passive exposure to aggression. Male Sprague-Dawley rats (N = 72) were passively exposed to either aggression or non-aggression acutely (1 day) or chronically (23 days). When observer rats were exposed to aggression chronically, they showed increased aggressive behavior and reduced D2R density in the bilateral AcbSh. On the other hand, exposure to aggression, regardless of exposure length, increased 5-HT1BR density in the bilateral BLA. Finally, low D2R in the AcbSh significantly interacted with high 5-HT1BR density in the BLA in predicting high levels of aggression in observer rats. Our results advance our understanding of the neurobiological mechanisms for observational learning of aggression, highlighting that dopamine-serotonin interaction, or AcbSh-BLA interaction, may contribute to a risk factor for aggression in observers who chronically witness aggressive interactions. PMID:25650085

  13. Distinct Neurochemical Adaptations Within the Nucleus Accumbens Produced by a History of Self-Administered vs Non-Contingently Administered Intravenous Methamphetamine

    Science.gov (United States)

    Lominac, Kevin D; Sacramento, Arianne D; Szumlinski, Karen K; Kippin, Tod E

    2012-01-01

    Methamphetamine is a highly addictive psychomotor stimulant yet the neurobiological consequences of methamphetamine self-administration remain under-characterized. Thus, we employed microdialysis in rats trained to self-administer intravenous (IV) infusions of methamphetamine (METH-SA) or saline (SAL) and a group of rats receiving non-contingent IV infusions of methamphetamine (METH-NC) at 1 or 21 days withdrawal to determine the dopamine and glutamate responses in the nucleus accumbens (NAC) to a 2 mg/kg methamphetamine intraperitoneal challenge. Furthermore, basal NAC extracellular glutamate content was assessed employing no net-flux procedures in these three groups at both time points. At both 1- and 21-day withdrawal points, methamphetamine elicited a rise in extracellular dopamine in SAL animals and this effect was sensitized in METH-NC rats. However, METH-SA animals showed a much greater sensitized dopamine response to the drug challenge compared with the other groups. Additionally, acute methamphetamine decreased extracellular glutamate in both SAL and METH-NC animals at both time-points. In contrast, METH-SA rats exhibited a modest and delayed rise in glutamate at 1-day withdrawal and this rise was sensitized at 21 days withdrawal. Finally, no net-flux microdialysis revealed elevated basal glutamate and increased extraction fraction at both withdrawal time-points in METH-SA rats. Although METH-NC rats exhibited no change in the glutamate extraction fraction, they exhibited a time-dependent elevation in basal glutamate levels. These data illustrate for the first time that a history of methamphetamine self-administration produces enduring changes in NAC neurotransmission and that non-pharmacological factors have a critical role in the expression of these methamphetamine-induced neurochemical adaptations. PMID:22030712

  14. The expression of Toll-like receptor 4, 7 and co-receptors in neurochemical sub-populations of rat trigeminal ganglion sensory neurons.

    Science.gov (United States)

    Helley, M P; Abate, W; Jackson, S K; Bennett, J H; Thompson, S W N

    2015-12-03

    The recent discovery that mammalian nociceptors express Toll-like receptors (TLRs) has raised the possibility that these cells directly detect and respond to pathogens with implications for either direct nociceptor activation or sensitization. A range of neuronal TLRs have been identified, however a detailed description regarding the distribution of expression of these receptors within sub-populations of sensory neurons is lacking. There is also some debate as to the composition of the TLR4 receptor complex on sensory neurons. Here we use a range of techniques to quantify the expression of TLR4, TLR7 and some associated molecules within neurochemically-identified sub-populations of trigeminal (TG) and dorsal root (DRG) ganglion sensory neurons. We also detail the pattern of expression and co-expression of two isoforms of lysophosphatidylcholine acyltransferase (LPCAT), a phospholipid remodeling enzyme previously shown to be involved in the lipopolysaccharide-dependent TLR4 response in monocytes, within sensory ganglia. Immunohistochemistry shows that both TLR4 and TLR7 preferentially co-localize with transient receptor potential vallinoid 1 (TRPV1) and purinergic receptor P2X ligand-gated ion channel 3 (P2X3), markers of nociceptor populations, within both TG and DRG. A gene expression profile shows that TG sensory neurons express a range of TLR-associated molecules. LPCAT1 is expressed by a proportion of both nociceptors and non-nociceptive neurons. LPCAT2 immunostaining is absent from neuronal profiles within both TG and DRG and is confined to non-neuronal cell types under naïve conditions. Together, our results show that nociceptors express the molecular machinery required to directly respond to pathogenic challenge independently from the innate immune system. Copyright © 2015 IBRO. Published by Elsevier Ltd. All rights reserved.

  15. Reinforcing and neurochemical effects of the “bath salts” constituents 3,4-methylenedioxypyrovalerone (MDPV) and 3,4-methylenedioxy-N-methylcathinone (methylone) in male rats

    Science.gov (United States)

    Schindler, Charles W.; Thorndike, Eric B.; Goldberg, Steven R.; Lehner, Kurt R.; Cozzi, Nicholas V.; Brandt, Simon D.; Baumann, Michael H.

    2015-01-01

    Rationale 3,4-Methylenedioxypyrovalerone (MDPV) and 3,4-methylenedioxy-N-methylcathinone (methylone) are synthetic drugs found in so-called “bath salts” products. Both drugs exert their effects by interacting with monoamine transporter proteins. MDPV is a potent uptake blocker at transporters for dopamine and norepinephrine while methylone is a non-selective releaser at transporters for dopamine, norepinephrine and serotonin (5-HT). Objectives We hypothesized that prominent 5-HT-releasing actions of methylone would render this drug less reinforcing than MDPV. Methods To test this hypothesis, we compared behavioral effects of MDPV and methylone using intravenous (i.v.) self-administration on a fixed-ratio 1 schedule in male rats. Additionally, neurochemical effects of the drugs were examined using in vivo microdialysis in nucleus accumbens, in a separate cohort of rats. Results MDPV self-administration (0.03 mg/kg/inj) was acquired rapidly, and reached 40 infusions per session, similar to the effects of cocaine (0.5 mg/kg/inj), by the end of training. By contrast, methylone self-administration (0.3 & 0.5 mg/kg/inj) was acquired slowly, and response rates only reached 20 infusions per session by the end of training. In dose substitution studies, MDPV and cocaine displayed typical inverted U-shaped dose-effect functions, but methylone did not. In vivo microdialysis revealed that i.v. MDPV (0.1 and 0.3 mg/kg) increased extracellular dopamine while i.v. methylone (1 and 3 mg/kg) increased extracellular dopamine and 5-HT. Conclusions Our findings support the hypothesis that elevations in extracellular 5-HT in the brain can dampen positive reinforcing effects of cathinone-type drugs. Nevertheless, MDPV and methylone are both self-administered by rats suggesting these drugs possess significant abuse liability in humans. PMID:26319160

  16. Reinforcing and neurochemical effects of the "bath salts" constituents 3,4-methylenedioxypyrovalerone (MDPV) and 3,4-methylenedioxy-N-methylcathinone (methylone) in male rats.

    Science.gov (United States)

    Schindler, Charles W; Thorndike, Eric B; Goldberg, Steven R; Lehner, Kurt R; Cozzi, Nicholas V; Brandt, Simon D; Baumann, Michael H

    2016-05-01

    3,4-Methylenedioxypyrovalerone (MDPV) and 3,4-methylenedioxy-N-methylcathinone (methylone) are synthetic drugs found in so-called "bath salts" products. Both drugs exert their effects by interacting with monoamine transporter proteins. MDPV is a potent uptake blocker at transporters for dopamine and norepinephrine while methylone is a non-selective releaser at transporters for dopamine, norepinephrine, and serotonin (5-HT). We hypothesized that prominent 5-HT-releasing actions of methylone would render this drug less reinforcing than MDPV. To test this hypothesis, we compared behavioral effects of MDPV and methylone using intravenous (i.v.) self-administration on a fixed-ratio 1 schedule in male rats. Additionally, neurochemical effects of the drugs were examined using in vivo microdialysis in nucleus accumbens, in a separate cohort of rats. MDPV self-administration (0.03 mg/kg/inj) was acquired rapidly and reached 40 infusions per session, similar to the effects of cocaine (0.5 mg/kg/inj), by the end of training. In contrast, methylone self-administration (0.3 and 0.5 mg/kg/inj) was acquired slowly, and response rates only reached 20 infusions per session by the end of training. In dose substitution studies, MDPV and cocaine displayed typical inverted U-shaped dose-effect functions, but methylone did not. In vivo microdialysis revealed that i.v. MDPV (0.1 and 0.3 mg/kg) increased extracellular dopamine while i.v. methylone (1 and 3 mg/kg) increased extracellular dopamine and 5-HT. Our findings support the hypothesis that elevations in extracellular 5-HT in the brain can dampen positive reinforcing effects of cathinone-type drugs. Nevertheless, MDPV and methylone are both self-administered by rats, suggesting these drugs possess significant abuse liability in humans.

  17. Developmental Neurotoxic Effects of Percutaneous Drug Delivery: Behavior and Neurochemical Studies in C57BL/6 Mice.

    Directory of Open Access Journals (Sweden)

    Huali Wu

    , 6% hydroquinone exposure elicited the most serious impairment of hippocampal structure and survival. The fact that higher doses of hydroquinone are associated with a greater risk of depression is further indication that hydroquinone is responsible for the development of depression. These above data demonstrated that chronic administration of different dermatology drugs contributed into common mental distress. This surprising discovery of chemical stressors stimulating the hippocampal dysfunction, paves the way for exciting areas of study on the cross-talk between the skin and the brain, as well as is suggesting how to develop effective and safe usage of dermatological drugs in daily practice.

  18. Developmental Neurotoxic Effects of Percutaneous Drug Delivery: Behavior and Neurochemical Studies in C57BL/6 Mice.

    Science.gov (United States)

    Wu, Huali; Feng, Junyi; Lv, Wenting; Huang, Qiaoling; Fu, Mengsi; Cai, Minxuan; He, Qiangqiang; Shang, Jing

    2016-01-01

    exposure elicited the most serious impairment of hippocampal structure and survival. The fact that higher doses of hydroquinone are associated with a greater risk of depression is further indication that hydroquinone is responsible for the development of depression. These above data demonstrated that chronic administration of different dermatology drugs contributed into common mental distress. This surprising discovery of chemical stressors stimulating the hippocampal dysfunction, paves the way for exciting areas of study on the cross-talk between the skin and the brain, as well as is suggesting how to develop effective and safe usage of dermatological drugs in daily practice.

  19. ATTENTION DEFICIT/HYPERACTIVITY DISORDER (ADHD)

    African Journals Online (AJOL)

    Enrique

    having attention deficit disorder without hyperactivity, girls outnumber boys. Genetic factors probably play a role in this disorder in more than 80% of cases. The pathophysiology in children with ADHD has been localised to 3 areas in the brain — the frontal lobe, its connection to the basal ganglia, and the relation- ship to the ...

  20. Intervertebral Disc Characteristic on Progressive Neurological Deficit

    Directory of Open Access Journals (Sweden)

    Farid Yudoyono

    2017-09-01

    Full Text Available Objective: To examine the intervertebral disc characteristic on magnetic resonance imaging (MRI in lumbar herniated disc (LHD patients with progressive neurological deficit. Methods: Patients were collected retrospectively from Dr. Hasan Sadikin General Hospital Database from 2011–2013 with LHD, had neurological deficit such as radiculopathy and cauda equine syndrome for less than four weeks with a positive sign confirmed by neurological examination and confirmatory with MRI examination. Results: A total of 14 patients with lumbar herniated disc disease (10 males, 4 females suffered from progressive neurological deficit with an average age of (52.07±10.9 years old. Early disc height was 9.38±0.5 mm and progressive neurological deficit state disc height was 4.03±0.53 mm, which were significantly different statisticaly (p<0.01. Symptoms of radiculopathy were seen in 11 patients and cauda equine syndrome in three patients. Modic changes grade 1 was found in five patients, grade 2 in eight patients,grade 3 in one patient, Pfirmman grade 2 in eleven patients and grade 3 in three patients. Thecal sac compression 1/3 compression was seen in four patients and 2/3 compression in ten patients. Conclusions: Neurosurgeon should raise concerns on the characteristic changes of intervertebral disc in magnetic resonance imaging examination to avoid further neural injury in lumbar herniated disc patients.

  1. Personality Correlates of Attention Deficit Hyperactivity Disorder.

    Science.gov (United States)

    Heilveil, Ira; Clark, Dona

    This study delineates personality correlates of attention deficit hyperactivity disorder (ADHD.) A standardized projective technique (the Roberts Apperception Test for Children (RATC) and the Conners Parent Rating Scale were administered to 52 ADHD children, ages 6-15. Results indicated that, when compared to the RATC standardization sample, ADHD…

  2. The Learning Disability of Attention Deficit Disorder.

    Science.gov (United States)

    Cherkes-Julkowski, Miriam; Stolzenberg, Jonathan

    1991-01-01

    Two discriminant function analyses were conducted to determine the cognitive/educational profile which differentiated 4 groups of 68 elementary/secondary level students: attention deficit disorder (ADD), with and without medication; learning disabilities (LD); and nonhandicapped. By treating the LD and nonmedicated ADD subjects as one group, a…

  3. Financing the U.S. Trade Deficit

    National Research Council Canada - National Science Library

    Jackson, James K

    2007-01-01

    The U.S. merchandise trade deficit is a part of the overall U.S. balance of payments, a summary statement of all economic transactions between the residents of the United States and the rest of the world, during a given period of time...

  4. Sensorimotor gating deficits in multiple system atrophy

    DEFF Research Database (Denmark)

    Zoetmulder, Marielle; Biernat, Heidi Bryde; Nikolic, Miki

    2014-01-01

    Prepulse inhibition (PPI) of the auditory blink reflex is a measure of sensorimotor gating, which reflects an organism's ability to filter out irrelevant sensory information. PPI has never been studied in patients with multiple system atrophy (MSA), although sensorimotor deficits are frequently...

  5. Medication Treatment for Attention Deficit Hyperactivity Disorder

    Science.gov (United States)

    Ryan, Joseph B.; Katsiyannis, Antonis; Hughes, Elizabeth M.

    2011-01-01

    Attention deficit hyperactivity disorder (ADHD) has become the most commonly diagnosed psychiatric disorder among school-age children. For more than half a century, physicians have prescribed medications to help manage behaviors such as hyperactivity, impulsivity, and inattention. Today, there is a growing consensus that ADHD is a biologically…

  6. Attention Deficit Hyperactivity Disorder: The Differential Diagnosis.

    Science.gov (United States)

    Weinberg, Warren A.; Emslie, Graham J.

    This paper presents information on the diagnostic criteria and management of disorders that may be wrongly identified as Attention Deficit Hyperactivity Disorder (ADHD) or may coexist with ADHD thus complicating identification and treatment. The disorders discussed are: depression, mania, primary disorder of vigilance, narcolepsy, developmental…

  7. Stigma in attention deficit hyperactivity disorder

    NARCIS (Netherlands)

    Müller, Kathi; Fuermaier, Anselm B M; Koerts, Janneke; Tucha, Lara

    Attention deficit hyperactivity disorder (ADHD) is a frequently diagnosed disorder in child- and adulthood with a high impact affecting multiple facets of social life. Therefore, patients suffering from ADHD are at high risk to be confronted with stigma, prejudices, and discrimination. A review of

  8. Did goethe describe attention deficit hyperactivity disorder?

    Science.gov (United States)

    Bonazza, Sara; Scaglione, Cesa; Poppi, Massimo; Rizzo, Giovanni

    2011-01-01

    As early as 1846, the typical symptoms of attention deficit hyperactivity disorder (ADHD) were described by Heinrich Hoffmann (1809-1894). However, in Goethe's masterpiece Faust (1832), the character of Euphorion strongly suggests ADHD diagnosis. Copyright © 2011 S. Karger AG, Basel.

  9. Park power deficit due to atmospheric stability

    DEFF Research Database (Denmark)

    Hansen, Kurt Schaldemose; Barthelmie, Rebecca; Ott, Søren

    The purpose of this paper is to present a power deficit analysis based on offshore wind farm measurements with respect to the atmospheric stability classification. The result is used to validate wind farm prediction models under different inflow and atmospheric stability conditions...

  10. Modafinil Trial in Attention Deficit Hyperactivity Disorder

    Directory of Open Access Journals (Sweden)

    J Gordon Millichap

    2005-12-01

    Full Text Available A film-coated tablet formulation of modafinil (ProvigilR was used to treat a total of 246 patients, ages 6 to 17 years, with attention deficit hyperactivity disorder (ADHD at the Massachusetts General Hospital, Boston, MA, and other centers.

  11. attention deficit hyperactivity disorder intervention: strategies

    African Journals Online (AJOL)

    Elizabeth

    The need for teachers' intervention strategies has been extensively discussed .... Emotional Disorder: More than half of pupils with attention-deficit hyperactivity disorder have accompanying disorders, including anxiety, depression, and conduct disorders. ... ADHD, the disorder does not affect intelligence. People with ADHD ...

  12. Aggression in children with attention-deficit/hyperactivity disorder.

    Science.gov (United States)

    King, Sara; Waschbusch, Daniel A

    2010-10-01

    Research shows that aggression is an important associated feature of attention-deficit/hyperactivity disorder (ADHD) and is important in understanding the impact of the disorder and its treatment. The occurrence of aggressive behavior in combination with ADHD does not appear to be spurious and the severity and/or presence of aggression and ADHD may significantly impact long-term prognosis. This article defines subtypes of aggression in relation to ADHD, identifies individual differences contributing to aggressive behavior in children with ADHD and discusses selected possible underlying mechanisms of aggression in ADHD, as well as current and emerging treatment approaches. Although aggressive behavior in children with ADHD is common, the reasons for this are not yet well understood. Multidisciplinary research should focus on investigating underlying mechanisms related to aggression in ADHD, as well as the utility of various treatment modalities.

  13. Memory deficits at 0.6 MPa ambient air pressure.

    Science.gov (United States)

    Tetzlaff, K; Leplow, B; Deistler, I; Ramm, G; Fehm-Wolfsdorf, G; Warninghoff, V; Bettinghausen, E

    1998-01-01

    We investigated the effects of an elevated ambient air pressure of 0.6 MPa on verbal memory performance. Twenty-four experienced divers were compressed in a dry hyperbaric chamber to pressures equivalent to 0.5 meters of seawater (msw) (n = 12) and 50 msw (n = 12). Verbal memory was assessed by free recall and recognition of visually presented word lists. The testing procedure specified learning and testing at surface, learning at surface and testing at depth, learning and testing at depth, and learning at depth and testing at surface. Non-specific stress was assessed by measurement of salivary cortisol, heart rate, and subjective stress before, during, and after the dives. The 50-msw dive group showed a significant decrease of free recall performance when the material was learned at depth (P stressors in the hyperbaric environment contributed to these deficits cannot be eliminated entirely.

  14. Sleep in Autism Spectrum Disorder and Attention Deficit Hyperactivity Disorder.

    Science.gov (United States)

    Singh, Kanwaljit; Zimmerman, Andrew W

    2015-06-01

    Sleep problems are common in autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD). Sleep problems in these disorders may not only worsen daytime behaviors and core symptoms of ASD and ADHD but also contribute to parental stress levels. Therefore, the presence of sleep problems in ASD and ADHD requires prompt attention and management. This article is presented in 2 sections, one each for ASD and ADHD. First, a detailed literature review about the burden and prevalence of different types of sleep disorders is presented, followed by the pathophysiology and etiology of the sleep problems and evaluation and management of sleep disorders in ASD and ADHD. Copyright © 2015 Elsevier Inc. All rights reserved.

  15. Heterogeneity of Developmental Dyscalculia: Cases with Different Deficit Profiles.

    Science.gov (United States)

    Träff, Ulf; Olsson, Linda; Östergren, Rickard; Skagerlund, Kenny

    2016-01-01

    Developmental Dyscalculia (DD) has long been thought to be a monolithic learning disorder that can be attributed to a specific neurocognitive dysfunction. However, recent research has increasingly recognized the heterogeneity of DD, where DD can be differentiated into subtypes in which the underlying cognitive deficits and neural dysfunctions may differ. The aim was to further understand the heterogeneity of developmental dyscalculia (DD) from a cognitive psychological perspective. Utilizing four children (8-9 year-old) we administered a comprehensive cognitive test battery that shed light on the cognitive-behavioral profile of each child. The children were compared against norm groups of aged-matched peers. Performance was then contrasted against predominant hypotheses of DD, which would also give insight into candidate neurocognitive correlates. Despite showing similar mathematical deficits, these children showed remarkable interindividual variability regarding cognitive profile and deficits. Two cases were consistent with the approximate number system deficit account and also the general magnitude-processing deficit account. These cases showed indications of having domain-general deficits as well. One case had an access deficit in combination with a general cognitive deficit. One case suffered from general cognitive deficits only. The results showed that DD cannot be attributed to a single explanatory factor. These findings support a multiple deficits account of DD and suggest that some cases have multiple deficits, whereas other cases have a single deficit. We discuss a previously proposed distinction between primary DD and secondary DD, and suggest hypotheses of dysfunctional neurocognitive correlates responsible for the displayed deficits.

  16. Oculomotor Anomalies in Attention-Deficit/Hyperactivity Disorder: Evidence for Deficits in Response Preparation and Inhibition

    Science.gov (United States)

    Mahone, E. Mark; Mostofsky, Stewart H.; Lasker, Adrian G.; Zee, David; Denckla, Martha B.

    2009-01-01

    Girls, but not boys, with attention deficit hyperactivity disorder (ADHD) have significantly longer visually guided saccades latencies. It is found that sex differences in children with ADHD extend beyond symptom presentation to the development of oculomotor control.

  17. Antidepressant-like activity of the endogenous amine, 1-methyl-1,2,3,4-tetrahydroisoquinoline in the behavioral despair test in the rat, and its neurochemical correlates: a comparison with the classical antidepressant, imipramine.

    Science.gov (United States)

    Wąsik, Agnieszka; Możdżeń, Edyta; Romańska, Irena; Michaluk, Jerzy; Antkiewicz-Michaluk, Lucyna

    2013-01-30

    Disturbances in noradrenergic and serotonergic transmissions have been postulated to form neurochemical background of depression. 1-Methyl-1,2,3,4-tetrahydroisoquinoline (1MeTIQ) is an endogenous substance which exhibits neuroprotective, antiaddictive and monoamine oxidase (MAO)-inhibiting properties. In the present study, we tested antidepressant-like effects of 1MeTIQ in comparison with the tricyclic antidepressant, imipramine in the forced swimming test in the rat. Additionally, in neurochemical studies, we estimated the rate of monoamine (dopamine, noradrenaline and serotonin) metabolism in the rat brain structures. The findings have shown that 1MeTIQ similarly to imipramine produced a dose-dependent antidepressant-like effect in the forced swimming test. The neurochemical data showed that 1MeTIQ produced a significant elevation of serotonin concentration in the brain structures with simultaneous reduction of its metabolite, 5-hydroxyindoleacetic acid (5-HIAA). Moreover, 1MeTIQ slightly increased noradrenaline level but induced a significant elevation of its metabolite, 3-metoxy-4-hydroxyphenylglycol (MHPG). Furthermore, 1MeTIQ affected also dopamine metabolism, and decreased the level of 3,4-dihydroxyphenylacetic acid (DOPAC) with a simultaneous significant increase in the concentration of 3-methoxytyramine (3-MT) in all investigated structures. Such mechanism of action leads to a decrease in the production of free radicals during MAO-dependent dopamine oxidation in the brain. In conclusion, we suggest that antidepressant-like activity of 1MeTIQ is based on the unique and complex mechanism of action in which the activation of monoaminergic systems and scavenging of free radicals plays a crucial role. 1MeTIQ as an endogenous compound may be beneficial from the clinical point of view as a new safer and more efficient antidepressant. Copyright © 2012 Elsevier B.V. All rights reserved.

  18. Cognitive deficits in the remitted state of unipolar depressive disorder

    DEFF Research Database (Denmark)

    Hasselbalch, Jacob; Knorr, Ulla; Hasselbalch, Steen Gregers

    2012-01-01

    Patients with unipolar depressive disorder may present with cognitive deficits in the remitted state, and the aim of the present study was to investigate whether cognitive deficits within specific cognitive domains are present....

  19. Attention-Deficit / Hyperactivity Disorder (ADHD): Data and Statistics

    Science.gov (United States)

    ... Controls Cancel Submit Search the CDC Attention-Deficit / Hyperactivity Disorder (ADHD) Note: Javascript is disabled or is not ... understand diagnosis and treatment patterns for Attention-Deficit/Hyperactivity Disorder (ADHD). On this page you can see information ...

  20. Children and Adults with Attention-Deficit/Hyperactivity Disorder

    Science.gov (United States)

    ... Annual Conference Children and Adults with Attention-Deficit/Hyperactivity Disorder (CHADD), is a national nonprofit organization that improves ... 2017 by Children and Adults with Attention-Deficit/Hyperactivity Disorder (CHADD). All Rights Reserved. Press Privacy Attention Magazine ...

  1. Evaluation of the double-deficit hypothesis in college students referred for learning difficulties.

    Science.gov (United States)

    Cirino, Paul T; Israelian, Marlyne K; Morris, Mary K; Morris, Robin D

    2005-01-01

    The present study explored the double-deficit hypothesis (DDH) in a sample of 146 college students with and without reading disabilities (RD). The results indicated that although both phonological awareness (PA) and visual naming speed (VNS) contributed to performance on measures of decoding and comprehension, their relative contribution was influenced both by the nature of the stimulus (word vs. nonword vs. text) and by the conditions of the task (timed vs. untimed). Similar results were obtained using an individual differences approach, or when between-group comparisons were made of individuals with deficits in PA or VNS. The relative representation of DDH subgroups in groups of adults with RD varied based on the classification criteria used to define RD. These results support the DDH, extend its applicability to adults, and have implications for diagnostic decision making.

  2. Human brain lesion-deficit inference remapped.

    Science.gov (United States)

    Mah, Yee-Haur; Husain, Masud; Rees, Geraint; Nachev, Parashkev

    2014-09-01

    Our knowledge of the anatomical organization of the human brain in health and disease draws heavily on the study of patients with focal brain lesions. Historically the first method of mapping brain function, it is still potentially the most powerful, establishing the necessity of any putative neural substrate for a given function or deficit. Great inferential power, however, carries a crucial vulnerability: without stronger alternatives any consistent error cannot be easily detected. A hitherto unexamined source of such error is the structure of the high-dimensional distribution of patterns of focal damage, especially in ischaemic injury-the commonest aetiology in lesion-deficit studies-where the anatomy is naturally shaped by the architecture of the vascular tree. This distribution is so complex that analysis of lesion data sets of conventional size cannot illuminate its structure, leaving us in the dark about the presence or absence of such error. To examine this crucial question we assembled the largest known set of focal brain lesions (n = 581), derived from unselected patients with acute ischaemic injury (mean age = 62.3 years, standard deviation = 17.8, male:female ratio = 0.547), visualized with diffusion-weighted magnetic resonance imaging, and processed with validated automated lesion segmentation routines. High-dimensional analysis of this data revealed a hidden bias within the multivariate patterns of damage that will consistently distort lesion-deficit maps, displacing inferred critical regions from their true locations, in a manner opaque to replication. Quantifying the size of this mislocalization demonstrates that past lesion-deficit relationships estimated with conventional inferential methodology are likely to be significantly displaced, by a magnitude dependent on the unknown underlying lesion-deficit relationship itself. Past studies therefore cannot be retrospectively corrected, except by new knowledge that would render them redundant

  3. Infantile Autism: A Syndrome of Multiple Primary Deficits?

    Science.gov (United States)

    Goodman, Robert

    1989-01-01

    Consideration of underlying neurological and psychological deficits suggests that the autistic syndrome results from the coexistence of at least two distinct constellations of functional impairments: deficits in mechanical language skills, as in the developmental dysphasias; and deficits in social relatedness, play, and nonverbal communication, as…

  4. Testing the Double-Deficit Hypothesis in an Adult Sample

    Science.gov (United States)

    Miller, Carlin J.; Miller, Scott R.; Bloom, Juliana S.; Jones, Lauren; Lindstrom, William; Craggs, Jason; Garcia-Barrera, Mauricio; Semrud-Clikeman, Margaret; Gilger, Jeffrey W.; Hynd, George W.

    2006-01-01

    The double-deficit hypothesis of dyslexia posits that reading deficits are more severe in individuals with weaknesses in phonological awareness and rapid naming than in individuals with deficits in only one of these reading composite skills. In this study, the hypothesis was tested in an adult sample as a model of reading achievement. Participants…

  5. Speech-Perception-in-Noise Deficits in Dyslexia

    Science.gov (United States)

    Ziegler, Johannes C.; Pech-Georgel, Catherine; George, Florence; Lorenzi, Christian

    2009-01-01

    Speech perception deficits in developmental dyslexia were investigated in quiet and various noise conditions. Dyslexics exhibited clear speech perception deficits in noise but not in silence. "Place-of-articulation" was more affected than "voicing" or "manner-of-articulation." Speech-perception-in-noise deficits persisted when performance of…

  6. Nicotinic receptors and lurasidone-mediated reversal of phencyclidine-induced deficit in novel object recognition.

    Science.gov (United States)

    Miyauchi, Masanori; Neugebauer, Nichole M; Oyamada, Yoshihiro; Meltzer, Herbert Y

    2016-03-15

    Enhancement of cholinergic function via nicotinic acetylcholine (ACh) receptor (nAChR) agonism is a potential approach for the treatment of cognitive impairment associated with schizophrenia (CIAS). Some atypical antipsychotic drugs (AAPDs) enhance ACh release in rodent brain, indirectly stimulating these receptors. Here, we elucidate which nAChR subtypes mediate novel object recognition (NOR) in normal rats and contribute to the ability of the AAPD, lurasidone, to improve the NOR deficit in sub-chronic (sc) phencyclidine (PCP)-treated rats, a model for CIAS. The ability of lurasidone and nAChR ligands to reverse the scPCP-induced deficit in NOR was assessed in female, Long-Evans rats. The broad acting nAChR antagonist, mecamylamine (MEC), induced a NOR deficit in normal rats. The NOR deficit secondary to scPCP was reversed by either selective α4β2* nAChR agonism (A-85380) or α7 nAChRs agonism (PNU-282987); these effects were blocked by DHβE and MLA, selective antagonists of α4β2* and α7 nAChR, respectively. The ability of lurasidone to reverse the scPCP-induced NOR deficit was blocked by MEC, but not MLA or DHβE. However, sub-effective doses (SED) of either A-85380 or PNU-282987 potentiated the ability of SED lurasidone to reverse the scPCP-induced NOR deficit. These results identify both α4β2* and α7 nAChRs as candidates for enhancing the ability of lurasidone and other AAPDs, which increase the release of ACh, to improve CIAS. Copyright © 2016. Published by Elsevier B.V.

  7. Altering length and velocity feedback during a neuro-musculoskeletal simulation of normal gait contributes to hemiparetic gait characteristics

    National Research Council Canada - National Science Library

    Jansen, Karen; De Groote, Friedl; Aerts, Wouter; De Schutter, Joris; Duysens, Jacques; Jonkers, Ilse

    2014-01-01

    .... In this study a neuro-musculoskeletal model was developed to investigate the contribution of an increased length and velocity feedback and altered reflex modulation patterns to hemiparetic gait deficits...

  8. Social Cognition Deficits and Psychopathic Traits in Young People Seeking Mental Health Treatment

    OpenAIRE

    van Zwieten, Anita; Meyer, Johanna; Hermens, Daniel F.; Hickie, Ian B.; Hawes, David J.; Glozier, Nicholas; Naismith, Sharon L.; Scott, Elizabeth M.; Lee, Rico S. C.; Guastella, Adam J.

    2013-01-01

    Antisocial behaviours and psychopathic traits place an individual at risk for criminality, mental illness, substance dependence, and psychosocial dysfunction. Social cognition deficits appear to be associated with psychopathic traits and are believed to contribute to interpersonal dysfunction. Most research investigating the relationship of these traits with social cognition has been conducted either in children or adult forensic settings. We investigated whether psychopathic traits were asso...

  9. Repeated, Intermittent Social Defeat across the Entire Juvenile Period Resulted in Behavioral, Physiological, Hormonal, Immunological, and Neurochemical Alterations in Young Adult Male Golden Hamsters

    Science.gov (United States)

    Yu, Wei-Chun; Liu, Ching-Yi; Lai, Wen-Sung

    2016-01-01

    The developing brain is vulnerable to social defeat during the juvenile period. As complements of human studies, animal models of social defeat provide a straightforward approach to investigating the functional and neurobiological consequences of social defeats. Taking advantage of agonist behavior and social defeat in male golden hamster, a set of 6 experiments was conducted to investigate the consequences at multiple levels in young adulthood resulting from repeated, intermittent social defeats or “social threats” across the entire juvenile period. Male hamsters at postnatal day 28 (P28) were randomly assigned to either the social defeat, “social threat”, or arena control group, and they correspondingly received a series of nine social interaction trials (i.e., either social defeat, “social threat”, or arena control conditions) from P33 to P66. At the behavioral level (Experiment 1), we found that repeated social defeats (but not “social threats”) significantly impacted locomotor activity in the familiar context and social interaction in the familiar/unfamiliar social contexts. At the physiological and hormonal levels (Experiments 2 and 3), repeated social defeat significantly enhanced the cortisol and norepinephrine concentrations in blood. Enlargement of the spleen was also found in the social defeat and “social threat” groups. At the immunological level (Experiment 4), the social defeat group showed lower levels of pro-inflammatory cytokines in the hypothalamus and hippocampus but higher concentration of IL-6 in the striatum compared to the other two groups. At the neurochemical level (Experiment 5), the socially defeated hamsters mainly displayed reductions of dopamine, dopamine metabolites, and 5-HT levels in the striatum and decreased level of 5-HT in the hippocampus. In Experiment 6, an increase in the spine density of hippocampal CA1 pyramidal neurons was specifically observed in the “social threat” group. Collectively, our

  10. Identification and distribution of neuronal nitric oxide synthase and neurochemical markers in the neuroepithelial cells of the gill and the skin in the giant mudskipper, Periophthalmodon schlosseri.

    Science.gov (United States)

    Zaccone, Giacomo; Lauriano, Eugenia Rita; Kuciel, Michał; Capillo, Gioele; Pergolizzi, Simona; Alesci, Alessio; Ishimatsu, Atsushi; Ip, Yuen Kwong; Icardo, Jose M

    2017-08-05

    Mudskippers are amphibious fishes living in mudflats and mangroves. These fishes hold air in their large buccopharyngeal-opercular cavities where respiratory gas exchange takes place via the gills and higher vascularized epithelium lining the cavities and also the skin epidermis. Although aerial ventilation response to changes in ambient gas concentration has been studied in mudskippers, the localization and distribution of respiratory chemoreceptors, their neurochemical coding and function as well as physiological evidence for the gill or skin as site for O2 and CO2 sensing are currently not known. In the present study we assessed the distribution of serotonin, acetylcholine, catecholamines and nitric oxide in the neuroepithelial cells (NECs) of the mudskipper gill and skin epithelium using immunohistochemistry and confocal microscopy. Colocalization studies showed that 5-HT is coexpressed with nNOS, Na+/K+-ATPase, TH and VAChT; nNOS is coexpressed with Na+/K+-ATPase and TH in the skin. In the gill 5-HT is coexpressed with nNOS and VAhHT and nNOS is coexpressed with Na+/K+-ATPase and TH. Acetylcholine is also expressed in chain and proximal neurons projecting to the efferent filament artery and branchial smooth muscle. The serotonergic cells c labeled with VAChT, nNOS and TH, thus indicating the presence of NEC populations and the possibility that these neurotransmitters (other than serotonin) may act as primary transmitters in the hypoxic reflex in fish gills. Immunolabeling with TH antibodies revealed that NECs in the gill and the skin are innervated by catecholaminergic nerves, thus suggesting that these cells are involved in a central control of branchial functions through their relationships with the sympathetic branchial nervous system. The Na+/K+-ATPase in mitochondria-rich cells (MRCs), which are most concentrated in the gill lamellar epithelium, is colabeled with nNOS and associated with TH nerve terminals. TH-immunopositive fine varicosities were also

  11. Very early language deficits in dyslexic children.

    Science.gov (United States)

    Scarborough, H S

    1990-12-01

    At 2 1/2 years of age, children who later developed reading disabilities were deficient in the length, syntactic complexity, and pronunciation accuracy of their spoken language, but not in lexical or speech discrimination skills. As 3-year-olds, these children began to show deficits in receptive vocabulary and object-naming abilities, and as 5-year-olds they exhibited weaknesses in object-naming, phonemic awareness, and letter-sound knowledge that have characterized kindergartners who became poor readers in other studies. These late preschool differences were related to subsequent reading status as well as to prior language skills, but early syntactic proficiency nevertheless accounted for some unique variance in grade 2 achievement when differences at age 5 were statistically controlled. The language deficits of dyslexic children were unrelated to maternal reading ability and were not observed in children from dyslexic families who became normal readers. The implications of the results for etiological issues are discussed.

  12. Neuropsychological deficits in patients with myocardial infarction

    Directory of Open Access Journals (Sweden)

    Sherin P. Antony

    2010-04-01

    Full Text Available Myocardial Infarction (MI, commonly known as a Heart Attack, remains a leading cause of death throughout the world. Studies have shown that patients, who had MI, have cognitive impairment affecting attention, problem solving, memory, visuospatial, executive function and even dementia. Since cognition and emotion are integral part of the disease, there are no focused studies addressing this issue in the Indian context. Hence the present study. The objective of the study was to determine the neuropsychological deficits in patients with MI and with MI after cardiac bypass surgery. The sample consisted of 30 patients, 15 MI and 15 MI after CABG. All patients were assessed on. a battery of Neuropsychological tests and Hamilton Rating Scale for depression, The findings revealed impairment in mental speed, sustained attention, Animal Fluency Test, Phonemic Fluency Test, verbal and visual working memory, planning, response inhibition, verbal and visual learning and memory. On comparison with MI patients CABG patients showed significant deficits in Planning.

  13. Traumatic knee extension deficit (the locked knee)

    DEFF Research Database (Denmark)

    Helmark, I C; Neergaard, K; Krogsgaard, M R

    2007-01-01

    In the present study we investigated the validity of magnetic resonance imaging (MRI) and arthroscopy in knees with acute, traumatic extension deficit (the "locked knee"), and evaluated whether arthroscopy of knees with no mechanical pathology could be avoided by MRI evaluation. The study consisted...... of 50 patients who had an acute, traumatic extension deficit of the knee. All patients were submitted to MRI prior to arthroscopy. Following MRI and surgery, standardized forms were filled out, attempting to objectify the findings. The orthopaedic surgeon was not aware of the MRI result prior to surgery......, the following results were calculated for the overall appearance of a lesion able to cause locking: Positive predictive value = 0.85, negative predictive value = 0.77, sensitivity = 0.95, specificity = 0.53. Two knees were erroneously evaluated with no mechanical locking at MRI (one bucket-handle lesion and one...

  14. Common Cognitive Deficits in Children with Attention-Deficit/Hyperactivity Disorder and Autism: Working Memory and Visual-Motor Integration

    Science.gov (United States)

    Englund, Julia A.; Decker, Scott L.; Allen, Ryan A.; Roberts, Alycia M.

    2014-01-01

    Cognitive deficits in working memory (WM) are characteristic features of Attention-Deficit/Hyperactivity Disorder (ADHD) and autism. However, few studies have investigated cognitive deficits using a wide range of cognitive measures. We compared children with ADHD ("n" = 49) and autism ("n" = 33) with a demographically matched…

  15. Stigma in attention deficit hyperactivity disorder

    OpenAIRE

    Mueller, Anna K.; Fuermaier, Anselm B. M.; Koerts, Janneke; Tucha, Lara

    2012-01-01

    Attention deficit hyperactivity disorder (ADHD) is a frequently diagnosed disorder in child- and adulthood with a high impact affecting multiple facets of social life. Therefore, patients suffering from ADHD are at high risk to be confronted with stigma, prejudices, and discrimination. A review of the empirical research in the field of ADHD with regard to stigma was performed. The findings of investigations in this field were clustered in different categories, including stigma in children wit...

  16. Enfranchisement and budget deficits: A theoretical note

    OpenAIRE

    Krogstrup, Signe; Wälti, Sébastien

    2009-01-01

    If women make different economic decisions than men on average, then an increase in women's influence in the political and economic spheres of society might change economic outcomes. In this note, we focus on the impact of female enfranchisement on fiscal policy outcomes. We present a simple median voter model and show that if women have different economic preferences than men, then female enfranchisement leads to a change in government budget deficits..

  17. The history of attention deficit hyperactivity disorder

    OpenAIRE

    Lange, Klaus W.; Reichl, Susanne; Lange, Katharina M.; Tucha, Lara; Tucha, Oliver

    2010-01-01

    The contemporary concept of attention deficit hyperactivity disorder (ADHD) as defined in the DSM-IV-TR (American Psychiatric Association 2000) is relatively new. Excessive hyperactive, inattentive, and impulsive children have been described in the literature since the nineteenth century. Some of the early depictions and etiological theories of hyperactivity were similar to current descriptions of ADHD. Detailed studies of the behavior of hyperactive children and increasing knowledge of brain...

  18. Bias and equivalence of the Strengths Use and Deficit COrrection Questionnaire in a South African context

    Directory of Open Access Journals (Sweden)

    Symen A. Brouwers

    2017-01-01

    Full Text Available Orientation: Developing personnel into skilled employees is a major focus of managers and companies. Doing this in a valid way in a cross-culturally diverse working environment may be challenging. It is, therefore, important to investigate the cultural consistency of new tools that assist managers in reaching these personnel development goals.Research purpose: Determine whether the Strengths Use and Deficit COrrection (SUDCO questionnaire is universally applicable across the Nguni, Sesotho and West-Germanic language groups in South Africa by evaluating it statistically for bias and equivalence.Motivation for the study: South African personnel management could gain valuable insights and outcomes when they aim to improve both strengths and weaknesses.Research design, approach and method: The study employed semi-stratified sampling. A sample (N = 658 of employees in the banking sector participated in the study. The research focused on psychometric properties relating to bias, structural equivalence and reliability.Main findings: A four-factor model fitted the data best. This model described perceived organisational support (POS for strengths use, POS for deficit correction, strengths-use behaviour and deficit-correction behaviour. A multi-group confirmatory factor analysis for the direct comparison of the SUDCO’s fit across the language groups (Nguni, Sesotho and WestGermanic showed the 33 were unbiased against any of the three language groups and structured into the same four latent constructs.Practical implications: In personnel development, employees and managers should understand the benefits of a combined strengths and deficit approach as relating to different language groups.Contribution: The study contributes to literature a cross-culturally validated measure for the assessment of strengths and deficits.

  19. Agaricus blazei extract abrogates rotenone-induced dopamine depletion and motor deficits by its anti-oxidative and anti-inflammatory properties in Parkinsonic mice.

    Science.gov (United States)

    Venkatesh Gobi, Veerappan; Rajasankar, Srinivasagam; Ramkumar, Muthu; Dhanalakshmi, Chinnasamy; Manivasagam, Thamilarasan; Justin Thenmozhi, Arokiasamy; Essa, Musthafa Mohamed; Chidambaram, Ranganathan; Kalandar, Ameer

    2017-06-19

    Neuroinflammation and oxidative damage are the two main malfactors that play an important role in the pathogenesis of experimental and clinical Parkinson's disease (PD). The current study was aimed to study the possible anti-oxidant and anti-inflammatory effects of the methanolic extract of Agaricus blazei (A. blazei) against rotenone-induced PD in mice. Male Albino mice were randomized and divided into the following groups: control, treated with rotenone (1 mg/kg/day), co-treated with rotenone and A. blazei (50, 100, and 200 mg/kg b.w.), and treated with A. blazei alone (200 mg/kg b.w.). After the end of the experimental period, behavioral studies, biochemical estimations, and protein expression patterns of inflammatory markers were studied. Rotenone treatment exhibited enhanced motor impairments, neurochemical deficits, oxidative stress, and inflammation, whereas oral administration of A. blazei extract attenuated the above-said indices. Even though further research is needed to prove its efficacy in clinical studies, the results of our study concluded that A. blazei extract offers a promising and new therapeutic lead for treatment of PD.

  20. Exceptional lexical skills but executive language deficits in school starters and young adults with Turners syndrome: implications for X chromosome effects on brain function.

    Science.gov (United States)

    Temple, Christine M; Shephard, Elizabeth E

    2012-03-01

    TS school starters had enhanced receptive and expressive language on standardised assessment (CELF-P) and enhanced rhyme judgements, spoonerisms, and lexical decision, indicating enhanced phonological skills and word representations. There was marginal but consistent advantage across lexico-semantic tasks. On executive tasks, speeded naming of numbers was impaired but not pictures. Young TS adults had enhanced naming and receptive vocabulary, indicating enhanced semantic skills. There were consistent deficits in executive language: phonemic oral fluency, rhyme fluency, speeded naming of pictures, numbers and colours; sentence completion requiring supression of prepotent responses. Haploinsufficiency of X-chromosome drives mechanisms that affect the anatomical and neurochemical development of the brain, resulting in enhanced temporal lobe aspects of language. These strengths co-exist with impaired development of frontal lobe executive language systems. This means not only that these elements of language can decouple in development but that their very independence is driven by mechanisms linked to the X-chromosome. Copyright © 2011 Elsevier Inc. All rights reserved.

  1. Medical Comorbidities in Attention Deficit Hyperactivity Disorder

    Directory of Open Access Journals (Sweden)

    Irem Yalug

    2009-09-01

    Full Text Available Attention Deficit Hyperactivity Disorder is one of the most common developmental disorders of childhood with a reported world-wide prevalence of 8 to 12 %. In studies conducted in our country the prevalence rates in community were reported to vary between 8.6 to 8.1 % while clinical prevalence rates were reported to vary between 8.6 to 29.44 %. Fifty to eighty percent of cases were reported to continue into adolescence while thirty to fifty percent may continue into adulthood. Attention deficit hyperactivity disorder is known to accompany subtle physical anomalies, allergic and neurologic disorders, obesity and eating disorders, traumatic injuries, risky sexual behavior, sleep disorders, substance and alcohol use, axis I and II disorders, occupational, legal and academic problems and increased treatment expenditures. Though the effects of this disorder continue throughout life, create burdens to the society along with its treatment as well as disabling the affected patients through their lives, and receive increasing attention in recent years, reviews focusing on problems associated with it are lacking. Therefore, this study aimed to summarize the results of previous studies conducted about medical comorbidities in attention deficit hyperactivity disorder.

  2. Word Learning Deficits in Children With Dyslexia.

    Science.gov (United States)

    Alt, Mary; Hogan, Tiffany; Green, Samuel; Gray, Shelley; Cabbage, Kathryn; Cowan, Nelson

    2017-04-14

    The purpose of this study is to investigate word learning in children with dyslexia to ascertain their strengths and weaknesses during the configuration stage of word learning. Children with typical development (N = 116) and dyslexia (N = 68) participated in computer-based word learning games that assessed word learning in 4 sets of games that manipulated phonological or visuospatial demands. All children were monolingual English-speaking 2nd graders without oral language impairment. The word learning games measured children's ability to link novel names with novel objects, to make decisions about the accuracy of those names and objects, to recognize the semantic features of the objects, and to produce the names of the novel words. Accuracy data were analyzed using analyses of covariance with nonverbal intelligence scores as a covariate. Word learning deficits were evident for children with dyslexia across every type of manipulation and on 3 of 5 tasks, but not for every combination of task/manipulation. Deficits were more common when task demands taxed phonology. Visuospatial manipulations led to both disadvantages and advantages for children with dyslexia. Children with dyslexia evidence spoken word learning deficits, but their performance is highly dependent on manipulations and task demand, suggesting a processing trade-off between visuospatial and phonological demands.

  3. Acetylcholinesterase inhibition ameliorates deficits in motivational drive

    Directory of Open Access Journals (Sweden)

    Martinowich Keri

    2012-03-01

    Full Text Available Abstract Background Apathy is frequently observed in numerous neurological disorders, including Alzheimer's and Parkinson's, as well as neuropsychiatric disorders including schizophrenia. Apathy is defined as a lack of motivation characterized by diminished goal-oriented behavior and self-initiated activity. This study evaluated a chronic restraint stress (CRS protocol in modeling apathetic behavior, and determined whether administration of an anticholinesterase had utility in attenuating CRS-induced phenotypes. Methods We assessed behavior as well as regional neuronal activity patterns using FosB immunohistochemistry after exposure to CRS for 6 h/d for a minimum of 21 d. Based on our FosB findings and recent clinical trials, we administered an anticholinesterase to evaluate attenuation of CRS-induced phenotypes. Results CRS resulted in behaviors that reflect motivational loss and diminished emotional responsiveness. CRS-exposed mice showed differences in FosB accumulation, including changes in the cholinergic basal forebrain system. Facilitating cholinergic signaling ameliorated CRS-induced deficits in initiation and motivational drive and rescued immediate early gene activation in the medial septum and nucleus accumbens. Conclusions Some CRS protocols may be useful for studying deficits in motivation and apathetic behavior. Amelioration of CRS-induced behaviors with an anticholinesterase supports a role for the cholinergic system in remediation of deficits in motivational drive.

  4. Olfactory deficits in boys with cleft palate.

    Science.gov (United States)

    Richman, R A; Sheehe, P R; McCanty, T; Vespasiano, M; Post, E M; Guzi, S; Wright, H

    1988-12-01

    An odor identification task was used to determine whether individuals with cleft palate (with or without cleft lip) also have an increased prevalence of olfactory deficits. Olfactory responses of 35 affected subjects (7 to 22 years of age) were compared with those of 68 subjects of comparable age without cleft palates. Subjects were requested to identify the smell of ten common household odors. They selected their responses from an alphabetized list of the test odorants. After a practice trial, the set of odorants was presented five times in randomized sequences. The percentage of correct responses increased with age for prepubertal and pubertal subjects without cleft palates. Although the olfactory scores of girls without cleft palates continued to increase after puberty, this trend was absent in boys. On the average, the girls with cleft palates, compared with only three of 34 boys without cleft palates, had olfactory scores less than 60% correct. There was no evidence of heterogeneity in the magnitude or direction of the relationship between any of the subtypes of cleft palate and olfactory dysfunction. In this study, cleft palate is more strongly associated with olfactory deficits in boys than in girls, suggesting the possibility that the deficit may be a sex-influenced trait.

  5. Vision Deficits in Adults with Down Syndrome

    Science.gov (United States)

    Krinsky-McHale, Sharon J.; Silverman, Wayne; Gordon, James; Devenny, Darlynne A.; Oley, Nancy; Abramov, Israel

    2013-01-01

    Background In individuals with Down syndrome virtually all structures of the eye have some abnormality which likely diminishes vision. We examined basic vision functions in adults with Down syndrome. Materials and Methods Participants completed a battery of psychophysical tests which probed a comprehensive array of visual functions. The performance of adults with Down syndrome was compared to younger and older adults without intellectual disability. Results Adults with Down syndrome had significant vision deficits; reduced sensitivity across spatial frequencies and temporal modulation rates, reduced stereopsis, impaired vernier acuity, and anomalies in colour discrimination. The pattern of deficits observed was similar to those seen by researchers examining adults with Alzheimer’s disease. Conclusions Our findings suggest that a common mechanism may be responsible for the pattern of deficits observed, possibly the presence of Alzheimer’s disease neuropathology in the visual association cortex. We also showed that individuals with mild to moderate intellectual disability are capable of participating in studies employing state-of-the-art psychophysical procedures. This has wider implications in terms of their ability to participate in research that use similar techniques. PMID:23784802

  6. Motor switching and motor adaptation deficits contribute to freezing of gait in Parkinson's disease

    NARCIS (Netherlands)

    Mohammadi, F.; Bruijn, S.M.; Vervoort, G.; van Wegen, E.E.H.; Kwakkel, G.; Verschueren, S.; Nieuwboer, A.

    2015-01-01

    Background. Patients with freezing of gait (FOG) have more difficulty with switching tasks as well as controlling the spatiotemporal parameters of gait than patients without FOG. Objective. To compare the ability of patients with and without FOG to adjust their gait to sudden speed switching and to

  7. Impaired Reelin-Dab1 Signaling Contributes to Neuronal Migration Deficits of Tuberous Sclerosis Complex

    Directory of Open Access Journals (Sweden)

    Uk Yeol Moon

    2015-08-01

    Full Text Available Tuberous sclerosis complex (TSC is associated with neurodevelopmental abnormalities, including defects in neuronal migration. However, the alterations in cell signaling mechanisms critical for migration and final positioning of neurons in TSC remain unclear. Our detailed cellular analyses reveal that reduced Tsc2 in newborn neurons causes abnormalities in leading processes of migrating neurons, accompanied by significantly delayed migration. Importantly, we demonstrate that Reelin-Dab1 signaling is aberrantly regulated in TSC mouse models and in cortical tubers from TSC patients owing to enhanced expression of the E3 ubiquitin ligase Cul5, a known mediator of pDab1 ubiquitination. Likewise, mTORC1 activation by Rheb overexpression generates similar neuronal and Reelin-Dab1 signaling defects, and directly upregulates Cul5 expression. Inhibition of mTORC1 by rapamycin treatment or by reducing Cul5 largely restores normal leading processes and positioning of migrating neurons. Thus, disrupted Reelin-Dab1 signaling is critically involved in the neuronal migration defects of TSC.

  8. Predicting attention-deficit/hyperactivity disorder severity from psychosocial stress and stress-response genes: a random forest regression approach

    NARCIS (Netherlands)

    Meer, D. van der; Hoekstra, P.J.; Donkelaar, M.M.J. van; Bralten, J.B.; Oosterlaan, J.; Heslenfeld, D.; Faraone, S.V; Franke, B.; Buitelaar, J.K.; Hartman, C.A.

    2017-01-01

    Identifying genetic variants contributing to attention-deficit/hyperactivity disorder (ADHD) is complicated by the involvement of numerous common genetic variants with small effects, interacting with each other as well as with environmental factors, such as stress exposure. Random forest regression

  9. Lifespan attention deficit/hyperactivity disorder and borderline personality disorder symptoms in female patients: A latent class approach.

    NARCIS (Netherlands)

    Dijk, F.E. van; Lappenschaar, M.; Kan, C.C.; Verkes, R.J.; Buitelaar, J.K.

    2011-01-01

    Attention-deficit/hyperactivity disorder (ADHD) and borderline personality disorder (BPD) are frequently comorbid. To contribute to a better understanding of the associations regularly found between ADHD and BPD, on the one hand, and the developmental pathways for these disorders, on the other hand,

  10. Cortical Inhibition in Attention Deficit Hyperactivity Disorder: New Insights from the Electroencephalographic Response to Transcranial Magnetic Stimulation

    Science.gov (United States)

    Bruckmann, Sarah; Hauk, Daniela; Roessner, Veit; Resch, Franz; Freitag, Christine M.; Kammer, Thomas; Ziemann, Ulf; Rothenberger, Aribert; Weisbrod, Matthias; Bender, Stephan

    2012-01-01

    Attention deficit hyperactivity disorder is one of the most frequent neuropsychiatric disorders in childhood. Transcranial magnetic stimulation studies based on muscle responses (motor-evoked potentials) suggested that reduced motor inhibition contributes to hyperactivity, a core symptom of the disease. Here we employed the N100 component of the…

  11. Motor Control in Children with ADHD and Non-Affected Siblings: Deficits Most Pronounced Using the Left Hand

    Science.gov (United States)

    Rommelse, Nanda N. J.; Altink, Marieke E.; Oosterlaan, Jaap; Buschgens, Cathelijne J. M.; Buitelaar, Jan; De Sonneville, Leo M. J.; Sergeant, Joseph A.

    2007-01-01

    Background: Attention-deficit/hyperactivity disorder (ADHD) is strongly influenced by heritability. Identifying heritable vulnerability traits (endophenotypes) that mark a relatively high risk of developing the disorder can contribute to the identification of risk genes. A fruitful area for the search for such endophenotypes may be motor control…

  12. Attention Mechanisms in Children with Anxiety Disorders and in Children with Attention Deficit Hyperactivity Disorder: Implications for Research and Practice

    Science.gov (United States)

    Weissman, Adam S.; Chu, Brian C.; Reddy, Linda A.; Mohlman, Jan

    2012-01-01

    Inattention is among the most commonly referred problems for school-aged youth. Research suggests distinct mechanisms may contribute to attention problems in youth with anxiety disorders versus youth with attention deficit hyperactivity disorder (ADHD). This study compared children (8-17 years) with anxiety disorders (n = 24) and children (8-16…

  13. Comorbid attention deficit hyperactivity disorder and substance use disorder complexity and chronicity in treatment-seeking adults

    NARCIS (Netherlands)

    Young, Jesse Tyler; Carruthers, Susan; Kaye, Sharlene; Allsop, Steve; Gilsenan, Joanne; Degenhardt, Louisa; van de Glind, Geurt; van den Brink, Wim; Preen, David

    2015-01-01

    Attention deficit hyperactivity disorder (ADHD) is a known risk factor for substance use disorder (SUD); however, the potential additive contribution of comorbid ADHD to drug-specific dependence in SUD populations is largely unknown. The current study aimed to assess this association between ADHD

  14. Neurochemical Profile of Dementia Pugilistica

    OpenAIRE

    Kokjohn, Tyler A.; Maarouf, Chera L.; Daugs, Ian D.; Hunter, Jesse M.; Charisse M Whiteside; Malek-Ahmadi, Michael; Rodriguez, Emma; Kalback, Walter; Jacobson, Sandra A.; Sabbagh, Marwan N; Beach, Thomas G; Roher, Alex E.

    2013-01-01

    Dementia pugilistica (DP), a suite of neuropathological and cognitive function declines after chronic traumatic brain injury (TBI), is present in approximately 20% of retired boxers. Epidemiological studies indicate TBI is a risk factor for neurodegenerative disorders including Alzheimer disease (AD) and Parkinson disease (PD). Some biochemical alterations observed in AD and PD may be recapitulated in DP and other TBI persons. In this report, we investigate long-term biochemical changes in th...

  15. Windows to the soul: vision science as a tool for studying biological mechanisms of information processing deficits in schizophrenia.

    Science.gov (United States)

    Yoon, Jong H; Sheremata, Summer L; Rokem, Ariel; Silver, Michael A

    2013-10-31

    Cognitive and information processing deficits are core features and important sources of disability in schizophrenia. Our understanding of the neural substrates of these deficits remains incomplete, in large part because the complexity of impairments in schizophrenia makes the identification of specific deficits very challenging. Vision science presents unique opportunities in this regard: many years of basic research have led to detailed characterization of relationships between structure and function in the early visual system and have produced sophisticated methods to quantify visual perception and characterize its neural substrates. We present a selective review of research that illustrates the opportunities for discovery provided by visual studies in schizophrenia. We highlight work that has been particularly effective in applying vision science methods to identify specific neural abnormalities underlying information processing deficits in schizophrenia. In addition, we describe studies that have utilized psychophysical experimental designs that mitigate generalized deficit confounds, thereby revealing specific visual impairments in schizophrenia. These studies contribute to accumulating evidence that early visual cortex is a useful experimental system for the study of local cortical circuit abnormalities in schizophrenia. The high degree of similarity across neocortical areas of neuronal subtypes and their patterns of connectivity suggests that insights obtained from the study of early visual cortex may be applicable to other brain regions. We conclude with a discussion of future studies that combine vision science and neuroimaging methods. These studies have the potential to address pressing questions in schizophrenia, including the dissociation of local circuit deficits vs. impairments in feedback modulation by cognitive processes such as spatial attention and working memory, and the relative contributions of glutamatergic and GABAergic deficits.

  16. Auditory and Visual Working Memory Functioning in College Students with Attention-Deficit/Hyperactivity Disorder and/or Learning Disabilities.

    Science.gov (United States)

    Liebel, Spencer W; Nelson, Jason M

    2017-12-01

    We investigated the auditory and visual working memory functioning in college students with attention-deficit/hyperactivity disorder, learning disabilities, and clinical controls. We examined the role attention-deficit/hyperactivity disorder subtype status played in working memory functioning. The unique influence that both domains of working memory have on reading and math abilities was investigated. A sample of 268 individuals seeking postsecondary education comprise four groups of the present study: 110 had an attention-deficit/hyperactivity disorder diagnosis only, 72 had a learning disability diagnosis only, 35 had comorbid attention-deficit/hyperactivity disorder and learning disability diagnoses, and 60 individuals without either of these disorders comprise a clinical control group. Participants underwent a comprehensive neuropsychological evaluation, and licensed psychologists employed a multi-informant, multi-method approach in obtaining diagnoses. In the attention-deficit/hyperactivity disorder only group, there was no difference between auditory and visual working memory functioning, t(100) = -1.57, p = .12. In the learning disability group, however, auditory working memory functioning was significantly weaker compared with visual working memory, t(71) = -6.19, p attention-deficit/hyperactivity disorder only group, there were no auditory or visual working memory functioning differences between participants with either a predominantly inattentive type or a combined type diagnosis. Visual working memory did not incrementally contribute to the prediction of academic achievement skills. Individuals with attention-deficit/hyperactivity disorder did not demonstrate significant working memory differences compared with clinical controls. Individuals with a learning disability demonstrated weaker auditory working memory than individuals in either the attention-deficit/hyperactivity or clinical control groups.

  17. Spatiotemporal postural control deficits are present in those with chronic ankle instability

    Directory of Open Access Journals (Sweden)

    McKeon Patrick O

    2008-06-01

    Full Text Available Abstract Background Postural control deficits have been purported to be a potential contributing factor in chronic ankle instability (CAI. Summary forceplate measures such as center of pressure velocity and area have not consistently detected postural control deficits associated with CAI. A novel measurement technique derived from the dynamical systems theory of motor control known as Time-to-boundary (TTB has shown promise in detecting deficits in postural control related to chronic ankle instability (CAI. In a previous study, TTB deficits were detected in a sample of females with CAI. The purpose of this study was to examine postural control in sample of males and females with and without CAI using TTB measures. Methods This case-control study was performed in a research laboratory. Thirty-two subjects (18 males, 14 females with self-reported CAI were recruited and matched to healthy controls. All subjects performed three, ten-second trials of single-limb stance on a forceplate with eyes open and eyes closed. Main outcome measures included the TTB absolute minimum (s, mean of TTB minima (s, and standard deviation of TTB minima (s in the anteroposterior and mediolateral directions. A series of group by gender analyses of variance were conducted to evaluate the differences in postural control for all TTB variables separately with eyes open and eyes closed. Results There were no significant group by gender interactions or gender main effects for any of the measures. There, however, significant group main effects for 4 of the 6 measures with eyes closed as the CAI group demonstrated significant deficits in comparison to the control group. There were no significant differences between groups in any of the TTB measures with eyes open. Conclusion TTB deficits were present in the CAI group compared to the control group. These deficits were detected with concurrent removal of visual input. CAI may place significantly greater constraints on the

  18. Chronic caffeine treatment during prepubertal period confers long-term cognitive benefits in adult spontaneously hypertensive rats (SHR), an animal model of attention deficit hyperactivity disorder (ADHD).

    Science.gov (United States)

    Pires, Vanessa A; Pamplona, Fabrício A; Pandolfo, Pablo; Prediger, Rui D S; Takahashi, Reinaldo N

    2010-12-20

    The spontaneously hypertensive rat (SHR) is frequently used as an experimental model for the study of attention deficit hyperactivity disorder (ADHD) since it displays behavioural and neurochemical features of ADHD. Increasing evidence suggests that caffeine might represent an important therapeutic tool for the treatment of ADHD and we recently demonstrated that the acute administration of caffeine improves several learning and memory impairments in adult SHR rats. Here we further evaluated the potential of caffeine in ADHD therapy. Female Wistar (WIS) and SHR rats were treated with caffeine (3mg/kg, i.p.) or methylphenidate (MPD, 2mg/kg, i.p.) for 14 consecutive days during the prepubertal period (post-natal days 25-38) and they were tested later in adulthood in the object-recognition task. WIS rats discriminated all the objects used, whereas SHR were not able to discriminate pairs of objects with subtle structural differences. Chronic treatment with caffeine or MPD improved the object-recognition deficits in SHR rats. Surprisingly, these treatments impaired the short-term object-recognition ability in adult WIS rats. The present drug effects are independent of changes in locomotor activity, arterial blood pressure and body weight in both rat strains. These findings suggest that chronic caffeine treatment during prepubertal period confers long-term cognitive benefits in discriminative learning impairments of SHR, suggesting caffeine as an alternative therapeutic strategy for the early management of ADHD symptoms. Nevertheless, our results also emphasize the importance of a correct diagnosis and the caution in the use of stimulant drugs such as caffeine and MPD during neurodevelopment since they can disrupt discriminative learning in non-ADHD phenotypes. Copyright 2010 Elsevier B.V. All rights reserved.

  19. Deficits in facial, body movement and vocal emotional processing in autism spectrum disorders.

    Science.gov (United States)

    Philip, R C M; Whalley, H C; Stanfield, A C; Sprengelmeyer, R; Santos, I M; Young, A W; Atkinson, A P; Calder, A J; Johnstone, E C; Lawrie, S M; Hall, J

    2010-11-01

    Previous behavioural and neuroimaging studies of emotion processing in autistic spectrum disorder (ASD) have focused on the use of facial stimuli. To date, however, no studies have examined emotion processing in autism across a broad range of social signals. This study addressed this issue by investigating emotion processing in a group of 23 adults with ASD and 23 age- and gender-matched controls. Recognition of basic emotions ('happiness', 'sadness', 'anger', disgust' and 'fear') was assessed from facial, body movement and vocal stimuli. The ability to make social judgements (such as approachability) from facial stimuli was also investigated. Significant deficits in emotion recognition were found in the ASD group relative to the control group across all stimulus domains (faces, body movements and voices). These deficits were seen across a range of emotions. The ASD group were also impaired in making social judgements compared to the control group and this correlated with impairments in basic emotion recognition. This study demonstrates that there are significant and broad-ranging deficits in emotion processing in ASD present across a range of stimulus domains and in the auditory and visual modality; they cannot therefore be accounted for simply in terms of impairments in face processing or in the visual modality alone. These results identify a core deficit affecting the processing of a wide range of emotional information in ASD, which contributes to the impairments in social function seen in people with this condition.

  20. The relationship between post-traumatic symptom severity and object relations deficits in persons with schizophrenia.

    Science.gov (United States)

    Chapleau, Kristine M; Bell, Morris D; Lysaker, Paul H

    2014-06-01

    The aim of this study was to determine if object relations deficits in people with schizophrenia spectrum disorders (i.e., schizophrenia and schizoaffective disorder) are related to co-morbid post-traumatic stress disorder (PTSD). Cross-sectional and correlational. Positive and Negative Syndrome Scale, Post-Traumatic Stress Disorder Checklist, and Bell Object Relations Inventory were administered to 60 people with schizophrenia in an outpatient setting. With four hierarchical regressions, we hypothesized that, controlling for schizophrenia symptoms, diagnosis type, and potential demographic features, PTSD symptoms would correlate with each of the four types of object relations deficits. All participants reported experiencing at least one traumatic experience. As predicted, PTSD symptoms were a significant predictor of alienation, insecure attachment, and egocentricity controlling for schizophrenia symptoms, diagnosis type, and demographic features. Against prediction, PTSD was not associated with Social Incompetence. If PTSD symptoms contribute to object relations deficits in persons with schizophrenia spectrum disorders, then interventions such as psychotherapy need to be developed to address PTSD symptoms in the treatment of these interpersonal deficits. © 2013 The British Psychological Society.

  1. Functional neural correlates of attentional deficits in amnestic mild cognitive impairment.

    Directory of Open Access Journals (Sweden)

    Nicholas T Van Dam

    Full Text Available Although amnestic mild cognitive impairment (aMCI; often considered a prodromal phase of Alzheimer's disease, AD is most recognized by its implications for decline in memory function, research suggests that deficits in attention are present early in aMCI and may be predictive of progression to AD. The present study used functional magnetic resonance imaging to examine differences in the brain during the attention network test between 8 individuals with aMCI and 8 neurologically healthy, demographically matched controls. While there were no significant behavioral differences between groups for the alerting and orienting functions, patients with aMCI showed more activity in neural regions typically associated with the networks subserving these functions (e.g., temporoparietal junction and posterior parietal regions, respectively. More importantly, there were both behavioral (i.e., greater conflict effect and corresponding neural deficits in executive control (e.g., less activation in the prefrontal and anterior cingulate cortices. Although based on a small number of patients, our findings suggest that deficits of attention, especially the executive control of attention, may significantly contribute to the behavioral and cognitive deficits of aMCI.

  2. Deficits in recognizing disgust facial expressions and Internet addiction: Perceived stress as a mediator.

    Science.gov (United States)

    Chen, Zhongting; Poon, Kai-Tak; Cheng, Cecilia

    2017-08-01

    Studies have examined social maladjustment among individuals with Internet addiction, but little is known about their deficits in specific social skills and the underlying psychological mechanisms. The present study filled these gaps by (a) establishing a relationship between deficits in facial expression recognition and Internet addiction, and (b) examining the mediating role of perceived stress that explains this hypothesized relationship. Ninety-seven participants completed validated questionnaires that assessed their levels of Internet addiction and perceived stress, and performed a computer-based task that measured their facial expression recognition. The results revealed a positive relationship between deficits in recognizing disgust facial expression and Internet addiction, and this relationship was mediated by perceived stress. However, the same findings did not apply to other facial expressions. Ad hoc analyses showed that recognizing disgust was more difficult than recognizing other facial expressions, reflecting that the former task assesses a social skill that requires cognitive astuteness. The present findings contribute to the literature by identifying a specific social skill deficit related to Internet addiction and by unveiling a psychological mechanism that explains this relationship, thus providing more concrete guidelines for practitioners to strengthen specific social skills that mitigate both perceived stress and Internet addiction. Copyright © 2017 Elsevier Ireland Ltd. All rights reserved.

  3. Methamphetamine treatment during development attenuates the dopaminergic deficits caused by subsequent high-dose methamphetamine administration.

    Science.gov (United States)

    McFadden, Lisa M; Hoonakker, Amanda J; Vieira-Brock, Paula L; Stout, Kristen A; Sawada, Nicole M; Ellis, Jonathan D; Allen, Scott C; Walters, Elliot T; Nielsen, Shannon M; Gibb, James W; Alburges, Mario E; Wilkins, Diana G; Hanson, Glen R; Fleckenstein, Annette E

    2011-08-01

    Administration of high doses of methamphetamine (METH) causes persistent dopaminergic deficits in both nonhuman preclinical models and METH-dependent persons. Noteworthy, adolescent [i.e., postnatal day (PND) 40] rats are less susceptible to this damage than young adult (PND90) rats. In addition, biweekly treatment with METH, beginning at PND40 and continuing throughout development, prevents the persistent dopaminergic deficits caused by a "challenge" high-dose METH regimen when administered at PND90. Mechanisms underlying this "resistance" were thus investigated. Results revealed that biweekly METH treatment throughout development attenuated both the acute and persistent deficits in VMAT2 function, as well as the acute hyperthermia, caused by a challenge METH treatment. Pharmacokinetic alterations did not appear to contribute to the protection afforded by the biweekly treatment. Maintenance of METH-induced hyperthermia abolished the protection against both the acute and persistent VMAT2-associated deficits suggesting that alterations in thermoregulation were caused by exposure of rats to METH during development. These findings suggest METH during development prevents METH-induced hyperthermia and the consequent METH-related neurotoxicity. Copyright © 2011 Wiley-Liss, Inc.

  4. LINGO-1 antibody ameliorates myelin impairment and spatial memory deficits in experimental autoimmune encephalomyelitis mice.

    Science.gov (United States)

    Sun, Jun-Jun; Ren, Qing-Guo; Xu, Lin; Zhang, Zhi-Jun

    2015-09-18

    More than 50% of multiple sclerosis patients develop cognitive impairment. However, the underlying mechanisms are still unclear, and there is no effective treatment. LINGO-1 (LRR and Ig domain containing NOGO receptor interacting protein 1) has been identified as an inhibitor of oligodendrocyte differentiation and myelination. Using the experimental autoimmune encephalomyelitis (EAE) mouse model, we assessed cognitive function at early and late stages of EAE, determined brain expression of myelin basic protein (MBP) and investigated whether the LINGO-1 antibody could restore deficits in learning and memory and ameliorate any loss of MBP. We found that deficits in learning and memory occurred in late EAE and identified decreased expression of MBP in the parahippocampal cortex (PHC) and fimbria-fornix. Moreover, the LINGO-1 antibody significantly improved learning and memory in EAE and partially restored MBP in PHC. Furthermore, the LINGO-1 antibody activated the AKT/mTOR signaling pathway regulating myelin growth. Our results suggest that demyelination in the PHC and fimbria-fornix might contribute to cognitive deficits and the LINGO-1 antibody could ameliorate these deficits by promoting myelin growth in the PHC. Our research demonstrates that LINGO-1 antagonism may be an effective approach to the treatment of the cognitive impairment of multiple sclerosis patients.

  5. Consequences of the Budget Deficit in the Current Crisis in Romania. Implications on the Labor Market

    Directory of Open Access Journals (Sweden)

    Gabriela MOLĂNESCU

    2011-02-01

    Full Text Available In the current economic activity conditions, in which the need of financial resources is usually higher than the existing funds, the elaborations of budgets at any level is one of the primary issues, particularly as regards the principle of budgetary balance. Approaches regarding sizing budgets deficits, means of financing and particularly sizing public debt get a series of touches of precise nature for different economies. Actual economic, financial, social and administrative conditions put up a series of problems which impose an extremely serious approach of the potential adverse impact by sizing of budget deficits and public debt over the real possibilities of noninflationary financing. In Romania, in the highly complex framework in which the economic activity takes place, in the attempt to show the place held by the budget deficit, a special role is assigned to determine the share of public financial deficit in the consolidated budget revenue and expenditure. Currently, knowledge and concern for reducing the budget deficit are still of great importance, especially as Romania is facing great difficulties in economic development. Amid deepening structural crisis phenomena, increasing budget deficits financed over a non-inflationary limits comes as an additional factor that contributes to imbalances of the economy. In addition, where budgetary expenditures are targeted to satisfy, primary, the redistribution function and to state subsidies, because of the lack of a real multiplier coefficient, the state budget deficit worsens. Influences such as introducing economic disturbance in the mechanisms which cause them to increase budget deficits can be summarized and grouped into two broad categories: economic influences and psychological influences. Regarding economic influences, we can say that they act strongly and strictly determined by how meanings used to cover budget deficit. The modalities used are subject to an analysis by direct or indirect

  6. Thermoregulation, scratch, itch and sleep deficits in children with eczema.

    Science.gov (United States)

    Camfferman, D; Short, M A; Kennedy, J D; Gold, M; Kohler, M; Lushington, K

    2016-09-01

    Successful sleep onset and maintenance is associated with a reduction in core temperature, facilitated by heat loss at the distal periphery. Problems with initiating and maintaining sleep in children with eczema may relate to impaired thermoregulatory mechanisms, which also contribute to itching and scratching. Our hypothesis was that nocturnal distal skin temperature in eczematous children would be lower than controls, and would also be related to poor sleep quality. We compared overnight polysomnography and distal (finger) and proximal (clavicle) skin temperature in 18 children with eczema and 15 controls (6-16 years). Children with eczema had longer periods of nocturnal wakefulness (mean [SD] = 88.8 [25.8] vs. 44.3 [35.6] min) and lower distal temperatures (34.1 [0.6] °C vs. 34.7 [0.4] °C) than controls, whereas proximal temperature and the distal-proximal gradient were not significantly different. In children with eczema, a higher distal temperature was associated with indicators of poor sleep quality, whereas lower distal temperature was related to more scratching events during sleep. In conclusion, our findings indicate complex interrelationships among eczema, thermoregulation and sleep, and further, that deficits in thermoregulatory mechanisms may contribute to sleep disturbances in children with eczema. Copyright © 2016 Elsevier B.V. All rights reserved.

  7. NIRS-based neurofeedback training in a virtual reality classroom for children with attention-deficit/hyperactivity disorder: study protocol for a randomized controlled trial

    OpenAIRE

    Blume, Friederike; Hudak, Justin; Dresler, Thomas; Ehlis, Ann-Christine; K?hnhausen, Jan; Renner, Tobias J; Gawrilow, Caterina

    2017-01-01

    Background Children with attention-deficit/hyperactivity disorder (ADHD) suffer from attention deficits, motor hyperactivity, and impulsive behaviour. These impairments are experienced at home, at school, and with friends. Functional imaging studies show that ADHD behaviour and impairments in executive functions (EFs) are mirrored by aberrant neurophysiological functioning. Moreover, several studies show that ADHD behaviour, impairments in EFs, and a lack of self-control contribute to poor sc...

  8. Neurocognitive processes of decision-making in adults with ADHD – Deficits in behavior and functional brain processing, and the effects of methylphenidate

    OpenAIRE

    Mowinckel, Athanasia Monika

    2017-01-01

    The work presented contributes to the further understanding and establishment of decision-making deficits in adults with ADHD. The meta-analysis in article I clearly identifies deficits in decision-making as an important factor in ADHD. The mechanistic, model-based fMRI analysis in article II provides strong evidence for reduced striatal reward coding in ADHD, and that treatment with methylphenidate at least partly remediates this abnormality. Lower-level cognitive functions are thus disrupte...

  9. Contribution of early environmental stress to alcoholism vulnerability

    Science.gov (United States)

    Campbell, Joannalee C.; Szumlinski, Karen K.; Kippin, Tod E.

    2011-01-01

    The most problematic aspects of alcohol abuse disorder are excessive alcohol consumption and the inability to refrain from alcohol consumption during attempted abstinence. The root causes that predispose certain individuals to these problems are poorly understood but are believed to be produced by a combination of genetic and environmental factors. Early environmental trauma alters neurodevelopmental trajectories that can predispose an individual to a number of neuropsychiatric disorders, including substance abuse. Prenatal stress (PNS) is a well-established protocol that produces perturbations in nervous system development, resulting in behavioral alterations that include hyperresponsiveness to stress, novelty, and psychomotor stimulant drugs (e.g., cocaine, amphetamine). Moreover, PNS animals exhibit enduring alterations in basal and cocaine-induced changes in dopamine and glutamate transmission within limbic structures, which exhibit pathology in drug addiction and alcoholism, suggesting that these alterations may contribute to an increased propensity to self-administer large amounts of drugs of abuse or to relapse after periods of drug withdrawal. Given that cocaine and alcohol have actions on common limbic neural substrates (albeit by different mechanisms), we hypothesized that PNS would elevate the motivation for, and consumption of, alcohol. Accordingly, we have found that male C57BL/6J mice subject to PNS exhibit higher operant responding and consume more alcohol during alcohol reinforcement as adults. Alterations in glutamate and dopamine neurotransmission within the forebrain structures appear to contribute to the PNS-induced predisposition to high alcohol intake and are induced by excessive alcohol intake. Accordingly, we are exploring the interactions between neurochemical changes produced by PNS and changes induced by consumption of alcohol in adulthood to model the biological bases of high vulnerability to alcohol abuse. PMID:19913199

  10. Amantadine Ameliorates Dopamine-Releasing Deficits and Behavioral Deficits in Rats after Fluid Percussion Injury

    Science.gov (United States)

    Huang, Eagle Yi-Kung; Tsui, Pi-Fen; Kuo, Tung-Tai; Tsai, Jing-Jr.; Chou, Yu-Ching; Ma, Hsin-I; Chiang, Yung-Hsiao; Chen, Yuan-Hao

    2014-01-01

    Aims To investigate the role of dopamine in cognitive and motor learning skill deficits after a traumatic brain injury (TBI), we investigated dopamine release and behavioral changes at a series of time points after fluid percussion injury, and explored the potential of amantadine hydrochloride as a chronic treatment to provide behavioral recovery. Materials and Methods In this study, we sequentially investigated dopamine release at the striatum and behavioral changes at 1, 2, 4, 6, and 8 weeks after fluid percussion injury. Rats subjected to 6-Pa cerebral cortical fluid percussion injury were treated by using subcutaneous infusion pumps filled with either saline (sham group) or amantadine hydrochloride, with a releasing rate of 3.6mg/kg/hour for 8 weeks. The dopamine-releasing conditions and metabolism were analyzed sequentially by fast scan cyclic voltammetry (FSCV) and high-pressure liquid chromatography (HPLC). Novel object recognition (NOR) and fixed-speed rotarod (FSRR) behavioral tests were used to determine treatment effects on cognitive and motor deficits after injury. Results Sequential dopamine-release deficits were revealed in 6-Pa-fluid-percussion cerebral cortical injured animals. The reuptake rate (tau value) of dopamine in injured animals was prolonged, but the tau value became close to the value for the control group after amantadine therapy. Cognitive and motor learning impairments were shown evidenced by the NOR and FSRR behavioral tests after injury. Chronic amantadine therapy reversed dopamine-release deficits, and behavioral impairment after fluid percussion injuries were ameliorated in the rats treated by using amantadine-pumping infusion. Conclusion Chronic treatment with amantadine hydrochloride can ameliorate dopamine-release deficits as well as cognitive and motor deficits caused by cerebral fluid-percussion injury. PMID:24497943

  11. Amantadine ameliorates dopamine-releasing deficits and behavioral deficits in rats after fluid percussion injury.

    Directory of Open Access Journals (Sweden)

    Eagle Yi-Kung Huang

    Full Text Available AIMS: To investigate the role of dopamine in cognitive and motor learning skill deficits after a traumatic brain injury (TBI, we investigated dopamine release and behavioral changes at a series of time points after fluid percussion injury, and explored the potential of amantadine hydrochloride as a chronic treatment to provide behavioral recovery. MATERIALS AND METHODS: In this study, we sequentially investigated dopamine release at the striatum and behavioral changes at 1, 2, 4, 6, and 8 weeks after fluid percussion injury. Rats subjected to 6-Pa cerebral cortical fluid percussion injury were treated by using subcutaneous infusion pumps filled with either saline (sham group or amantadine hydrochloride, with a releasing rate of 3.6 mg/kg/hour for 8 weeks. The dopamine-releasing conditions and metabolism were analyzed sequentially by fast scan cyclic voltammetry (FSCV and high-pressure liquid chromatography (HPLC. Novel object recognition (NOR and fixed-speed rotarod (FSRR behavioral tests were used to determine treatment effects on cognitive and motor deficits after injury. RESULTS: Sequential dopamine-release deficits were revealed in 6-Pa-fluid-percussion cerebral cortical injured animals. The reuptake rate (tau value of dopamine in injured animals was prolonged, but the tau value became close to the value for the control group after amantadine therapy. Cognitive and motor learning impairments were shown evidenced by the NOR and FSRR behavioral tests after injury. Chronic amantadine therapy reversed dopamine-release deficits, and behavioral impairment after fluid percussion injuries were ameliorated in the rats treated by using amantadine-pumping infusion. CONCLUSION: Chronic treatment with amantadine hydrochloride can ameliorate dopamine-release deficits as well as cognitive and motor deficits caused by cerebral fluid-percussion injury.

  12. Amantadine ameliorates dopamine-releasing deficits and behavioral deficits in rats after fluid percussion injury.

    Science.gov (United States)

    Huang, Eagle Yi-Kung; Tsui, Pi-Fen; Kuo, Tung-Tai; Tsai, Jing-Jr; Chou, Yu-Ching; Ma, Hsin-I; Chiang, Yung-Hsiao; Chen, Yuan-Hao

    2014-01-01

    To investigate the role of dopamine in cognitive and motor learning skill deficits after a traumatic brain injury (TBI), we investigated dopamine release and behavioral changes at a series of time points after fluid percussion injury, and explored the potential of amantadine hydrochloride as a chronic treatment to provide behavioral recovery. In this study, we sequentially investigated dopamine release at the striatum and behavioral changes at 1, 2, 4, 6, and 8 weeks after fluid percussion injury. Rats subjected to 6-Pa cerebral cortical fluid percussion injury were treated by using subcutaneous infusion pumps filled with either saline (sham group) or amantadine hydrochloride, with a releasing rate of 3.6 mg/kg/hour for 8 weeks. The dopamine-releasing conditions and metabolism were analyzed sequentially by fast scan cyclic voltammetry (FSCV) and high-pressure liquid chromatography (HPLC). Novel object recognition (NOR) and fixed-speed rotarod (FSRR) behavioral tests were used to determine treatment effects on cognitive and motor deficits after injury. Sequential dopamine-release deficits were revealed in 6-Pa-fluid-percussion cerebral cortical injured animals. The reuptake rate (tau value) of dopamine in injured animals was prolonged, but the tau value became close to the value for the control group after amantadine therapy. Cognitive and motor learning impairments were shown evidenced by the NOR and FSRR behavioral tests after injury. Chronic amantadine therapy reversed dopamine-release deficits, and behavioral impairment after fluid percussion injuries were ameliorated in the rats treated by using amantadine-pumping infusion. Chronic treatment with amantadine hydrochloride can ameliorate dopamine-release deficits as well as cognitive and motor deficits caused by cerebral fluid-percussion injury.

  13. Social Contributions in Romania

    Directory of Open Access Journals (Sweden)

    Attila Gyorgy

    2012-12-01

    Full Text Available Social contributions have an important impact on payroll policy. Also, social contributions represent a significant budgetary revenue item which can be viewed at the edge between taxation and insurance. Social contributions in Romania experienced many changes which ended in 2008. Nowadays, they are within a long transaction period towards partial externalization of the insurance activity to privately managed funds. The aim of this paper is to analyse the homogeneity of Romanian social security public scheme using annual data extracted from 2002-2009.The main findings reveal that social contributions reached the pinnacle of diversification, being too many, some of them with a small contribution rates; fiscal reforms which reduced contribution rates advantaged employers, and state will be interested to externalize this activity as far private sector will be able to assume this responsibility and the budgetary effects are acceptable for the public finance.

  14. [Adult attention deficit/hyperactivity disorder].

    Science.gov (United States)

    Laufkötter, R; Eichhammer, P; Hajak, G

    2004-08-19

    ADHD (attention deficit/hyperactivity disorder) in adults is a more complex pathological condition than ADHD seen in children and adolescents. The number of reports of impaired self-regulation are on the increase. Psychiatric comorbities are being found ever more frequently, and negative life experiences are coloring the clinical presentation to an ever greater extent. Therapeutic strategies involving the use of stimulants and antidepressants are often needed to pave the way for individual and group psychotherapy. Despite the fact that it is currently considered to be "fashionable", the diagnosis of ADHD is a clinically relevant and persisting psychological disorder.

  15. Sustained Perceptual Deficits from Transient Sensory Deprivation

    Science.gov (United States)

    Sanes, Dan H.

    2015-01-01

    Sensory pathways display heightened plasticity during development, yet the perceptual consequences of early experience are generally assessed in adulthood. This approach does not allow one to identify transient perceptual changes that may be linked to the central plasticity observed in juvenile animals. Here, we determined whether a brief period of bilateral auditory deprivation affects sound perception in developing and adult gerbils. Animals were reared with bilateral earplugs, either from postnatal day 11 (P11) to postnatal day 23 (P23) (a manipulation previously found to disrupt gerbil cortical properties), or from P23-P35. Fifteen days after earplug removal and restoration of normal thresholds, animals were tested on their ability to detect the presence of amplitude modulation (AM), a temporal cue that supports vocal communication. Animals reared with earplugs from P11-P23 displayed elevated AM detection thresholds, compared with age-matched controls. In contrast, an identical period of earplug rearing at a later age (P23-P35) did not impair auditory perception. Although the AM thresholds of earplug-reared juveniles improved during a week of repeated testing, a subset of juveniles continued to display a perceptual deficit. Furthermore, although the perceptual deficits induced by transient earplug rearing had resolved for most animals by adulthood, a subset of adults displayed impaired performance. Control experiments indicated that earplugging did not disrupt the integrity of the auditory periphery. Together, our results suggest that P11-P23 encompasses a critical period during which sensory deprivation disrupts central mechanisms that support auditory perceptual skills. SIGNIFICANCE STATEMENT Sensory systems are particularly malleable during development. This heightened degree of plasticity is beneficial because it enables the acquisition of complex skills, such as music or language. However, this plasticity comes with a cost: nervous system development

  16. Sleep Restores Daytime Deficits in Procedural Memory in Children with Attention-Deficit/Hyperactivity Disorder

    Science.gov (United States)

    Prehn-Kristensen, Alexander; Molzow, Ina; Munz, Manuel; Wilhelm, Ines; Muller, Kathrin; Freytag, Damaris; Wiesner, Christian D.; Baving, Lioba

    2011-01-01

    Sleep supports the consolidation of declarative and procedural memory. While prefrontal cortex (PFC) activity supports the consolidation of declarative memory during sleep, opposite effects of PFC activity are reported with respect to the consolidation of procedural memory during sleep. Patients with attention-deficit/hyperactivity disorder (ADHD)…

  17. How specific are executive functioning deficits in attention deficit hyperactivity disorder and autism?

    NARCIS (Netherlands)

    Geurts, H.M.; Verté, S.; Oosterlaan, J.; Roeyers, M.; Sergeant, J.A.

    2004-01-01

    Background: The objective of this study is to identify intact and deficient cognitive processes in children with attention deficit hyperactivity disorder (ADHD) and children with high functioning autism (HFA). Method: Three rigorously diagnosed groups of children aged between 6 and 12 years (54

  18. How specific are executive functioning deficits in attention deficit hyperactivity disorder and autism?

    NARCIS (Netherlands)

    Geurts, H.M.; Verté, S.; Oosterlaan, J.; Roeyers, M.; Sergeant, J.A.

    2003-01-01

    Background: The objective of this study is to identify intact and deficient cognitive processes in children with attention deficit hyperactivity disorder (ADHD) and children with high functioning autism (HFA). Method: Three rigorously diagnosed groups of children aged between 6 and 12 years (54

  19. Restraint and Cancellation: Multiple Inhibition Deficits in Attention Deficit Hyperactivity Disorder

    Science.gov (United States)

    Schachar, Russell; Logan, Gordon D.; Robaey, Philippe; Chen, Shirley; Ickowicz, Abel; Barr, Cathy

    2007-01-01

    We used variations of the stop signal task to study two components of motor response inhibition--the ability to withhold a strong response tendency (restraint) and the ability to cancel an ongoing action (cancellation)--in children with a diagnosis of attention deficit hyperactivity disorder (ADHD) and in non-ADHD controls of similar age (ages…

  20. A Cognitive Distortions and Deficits Model of Suicide Ideation.

    Science.gov (United States)

    Fazakas-DeHoog, Laura L; Rnic, Katerina; Dozois, David J A

    2017-05-01

    Although cognitive distortions and deficits are known risk factors for the development and escalation of suicide ideation and behaviour, no empirical work has examined how these variables interact to predict suicide ideation. The current study proposes an integrative model of cognitive distortions (hopelessness and negative evaluations of self and future) and deficits (problem solving deficits, problem solving avoidance, and cognitive rigidity). To test the integrity of this model, a sample of 397 undergraduate students completed measures of deficits, distortions, and current suicide ideation. A structural equation model demonstrated excellent fit, and findings indicated that only distortions have a direct effect on suicidal thinking, whereas cognitive deficits may exert their effects on suicide ideation via their reciprocal relation with distortions. Findings underscore the importance of both cognitive distortions and deficits for understanding suicidality, which may have implications for preventative efforts and treatment.

  1. Budget Deficit and Macroeconomics Fundamentals: The case of Azerbaijan

    Directory of Open Access Journals (Sweden)

    Kahnim Farajova

    2011-08-01

    Full Text Available In recent years, the emergence of rising budget deficit is the main reason forcing economists to investigate the reasons for changes in fiscal balances. The purpose of the paper is to investigate the relationship between budget deficit and macroeconomic fundamentals using data from Azerbaijan. The empirical analysis applies ARDL Cointegration methodology in conjunction with Granger causality tests to provide evidence for both the long and short run dynamics between the variables involved in the analysis. Using the Error Correction specification, there was found evidence of long-run causality running from current account, real interest rate, GDP, inflation and exchange rate to budget deficit. There was also found evidence of short-run Granger causal effects running from current account and real interest rate towards budget deficit and a rather weak causal effect from inflation to budget deficit. However, there is no short – run causality running from interest rate to budget deficit.

  2. Are auditory and visual processing deficits related to developmental dyslexia?

    Science.gov (United States)

    Georgiou, George K; Papadopoulos, Timothy C; Zarouna, Elena; Parrila, Rauno

    2012-05-01

    The purpose of this study was to examine if children with dyslexia learning to read a consistent orthography (Greek) experience auditory and visual processing deficits and if these deficits are associated with phonological awareness, rapid naming speed and orthographic processing. We administered measures of general cognitive ability, phonological awareness, orthographic processing, short-term memory, rapid automatized naming, auditory and visual processing, and reading fluency to 21 Grade 6 children with dyslexia, 21 chronological age-matched controls and 20 Grade 3 reading age-matched controls. The results indicated that the children with dyslexia did not experience auditory processing deficits, but about half of them showed visual processing deficits. Both orthographic processing and rapid automatized naming deficits were associated with dyslexia in our sample, but it is less clear that they were associated with visual processing deficits. Copyright © 2012 John Wiley & Sons, Ltd.

  3. A Cognitive Distortions and Deficits Model of Suicide Ideation

    Directory of Open Access Journals (Sweden)

    Laura L. Fazakas-DeHoog

    2017-05-01

    Full Text Available Although cognitive distortions and deficits are known risk factors for the development and escalation of suicide ideation and behaviour, no empirical work has examined how these variables interact to predict suicide ideation. The current study proposes an integrative model of cognitive distortions (hopelessness and negative evaluations of self and future and deficits (problem solving deficits, problem solving avoidance, and cognitive rigidity. To test the integrity of this model, a sample of 397 undergraduate students completed measures of deficits, distortions, and current suicide ideation. A structural equation model demonstrated excellent fit, and findings indicated that only distortions have a direct effect on suicidal thinking, whereas cognitive deficits may exert their effects on suicide ideation via their reciprocal relation with distortions. Findings underscore the importance of both cognitive distortions and deficits for understanding suicidality, which may have implications for preventative efforts and treatment.

  4. Motivation deficit in ADHD is associated with dysfunction of the dopamine reward pathway

    Energy Technology Data Exchange (ETDEWEB)

    Volkow, N.D.; Wang, G.; Volkow, N.D.; Wang, G.-J.; Newcorn, J.H.; Kollins, S.H.; Wigal, T.L.; Telang, F.; Folwer, J.S.; Goldstein, R.Z.; Klein, N.; Logan, J.; Wong, C.; Swanson, J.M.

    2010-08-17

    Attention-deficit hyperactivity disorder (ADHD) is typically characterized as a disorder of inattention and hyperactivity/impulsivity but there is increasing evidence of deficits in motivation. Using positron emission tomography (PET), we showed decreased function in the brain dopamine reward pathway in adults with ADHD, which, we hypothesized, could underlie the motivation deficits in this disorder. To evaluate this hypothesis, we performed secondary analyses to assess the correlation between the PET measures of dopamine D2/D3 receptor and dopamine transporter availability (obtained with [{sup 11}C]raclopride and [{sup 11}C]cocaine, respectively) in the dopamine reward pathway (midbrain and nucleus accumbens) and a surrogate measure of trait motivation (assessed using the Achievement scale on the Multidimensional Personality Questionnaire or MPQ) in 45 ADHD participants and 41 controls. The Achievement scale was lower in ADHD participants than in controls (11 {+-} 5 vs 14 {+-} 3, P < 0.001) and was significantly correlated with D2/D3 receptors (accumbens: r = 0.39, P < 0.008; midbrain: r = 0.41, P < 0.005) and transporters (accumbens: r = 0.35, P < 0.02) in ADHD participants, but not in controls. ADHD participants also had lower values in the Constraint factor and higher values in the Negative Emotionality factor of the MPQ but did not differ in the Positive Emotionality factor - and none of these were correlated with the dopamine measures. In ADHD participants, scores in the Achievement scale were also negatively correlated with symptoms of inattention (CAARS A, E and SWAN I). These findings provide evidence that disruption of the dopamine reward pathway is associated with motivation deficits in ADHD adults, which may contribute to attention deficits and supports the use of therapeutic interventions to enhance motivation in ADHD.

  5. Assessing the organisational and individual strengths use and deficit improvement amongst sport coaches

    Directory of Open Access Journals (Sweden)

    Frederick W. Stander

    2013-03-01

    Full Text Available Orientation: The orientation of this study is towards strengths use and deficit improvement and the relationship with engagement.Research purpose: To (1 determine whether adapted versions of the Strengths Use and Deficit Improvement Questionnaire (SUDIQ and Utrecht Work Engagement Scale (UWES are valid and reliable, (2 determine the relationship of the SUDIQ dimensions in the nomological net, and (3 test a structural model.Motivation for the study: To gain a better understanding of the outcomes of following a balanced approach within a sport coaching context.Research design, approach and method: A cross-sectional research approach was used. An availability sample (N = 364 of teachers occupying roles as sport coaches from various schools across three provinces in South Africa was used. Structural equation modelling was used to test the factor structures and the structural model.Main findings: The results indicated a valid factor structure for the adapted SUDIQ and UWES. Relationships between the SUDIQ dimensions and job and personal resources were positive and significant. Individual strengths use was the strongest predictor of engagement. Individual deficit improvement and organisational strengths use were also significant predictors. Organisational deficit improvement did not significantly predict engagement.Practical/managerial implications: Evidence suggests the adapted SUDIQ and UWES can be utilised effectively in a sport coaching environment. Organisational strengths use is also important in managing engagement levels of sport coaches.Contribution/value-add: Valid and reliable measures were provided for use in a sport coaching environment. It substantiates the outcomes that can be gained by following a combined approach based on strength and deficit.

  6. Neuromuscular Control Deficits and the Risk of Subsequent Injury after a Concussion: A Scoping Review.

    Science.gov (United States)

    Howell, David R; Lynall, Robert C; Buckley, Thomas A; Herman, Daniel C

    2018-02-17

    An emerging area of research has identified that an increased risk of musculoskeletal injury may exist upon returning to sports after a sport-related concussion. The mechanisms underlying this recently discovered phenomenon, however, remain unknown. One theorized reason for this increased injury risk includes residual neuromuscular control deficits that remain impaired despite clinical recovery. Thus, the objectives of this review were: (1) to summarize the literature examining the relationship between concussion and risk of subsequent injury and (2) to summarize the literature for one mechanism with a theorized association with this increased injury risk, i.e., neuromuscular control deficits observed during gait after concussion under dual-task conditions. Two separate reviews were conducted consistent with both specified objectives. Studies published before 9 December, 2016 were identified using PubMed, Web of Science, and Academic Search Premier (EBSCOhost). Inclusion for the objective 1 search included dependent variables of quantitative measurements of musculoskeletal injury after concussion. Inclusion criteria for the objective 2 search included dependent variables pertaining to gait, dynamic balance control, and dual-task function. A total of 32 studies were included in the two reviews (objective 1 n = 10, objective 2 n = 22). According to a variety of study designs, athletes appear to have an increased risk of sustaining a musculoskeletal injury following a concussion. Furthermore, dual-task neuromuscular control deficits may continue to exist after patients report resolution of concussion symptoms, or perform normally on other clinical concussion tests. Therefore, musculoskeletal injury risk appears to increase following a concussion and persistent motor system and attentional deficits also seem to exist after a concussion. While not yet experimentally tested, these motor system and attentional deficits may contribute to the risk of sustaining a

  7. Deficit Irrigation and Fertility Effects on NO3-N Exports from St. Augustinegrass.

    Science.gov (United States)

    Fontanier, Charles H; Aitkenhead-Peterson, Jacqueline A; Wherley, Benjamin G; White, Richard H; Thomas, James C; Dwyer, Phil

    2017-07-01

    Proper management of turfgrass systems is critical for reducing the risk of nutrient loss and protecting urban surface waters. In the southern United States, irrigation can be the most significant management practice regulating the biogeochemical and hydrological cycles of turfgrass systems. A turfgrass runoff research facility was used to assess the effects of deficit irrigation and fertilizer applications on turfgrass canopy cover and nitrate-N (NO-N) exports in runoff from St. Augustinegrass [Stenotaphrum secundatum (Walt.) Kuntze] turf over a 2-yr period. Treatments were arranged as a randomized complete block design having eight combinations of irrigation (100, 75, or 50% of estimated turfgrass water requirements) and fertility level (0, 88, and 176 kg N ha yr). Runoff from 31 rainfall events and one irrigation excess event were used to estimate annual and seasonal NO-N exports. The majority of annual NO-N exports occurred during the late winter and spring. Deficit irrigation reduced summer and early autumn runoff volumes. Lower summer and autumn runoff volumes (from deficit irrigation) coincided with reduced NO-N exports from runoff during Year 1. Deficit irrigation combined with fertilizer applications increased runoff [NO-N] in Year 2, suggesting that the previous year's export reduction contributed to higher N accumulation in the system and thus a higher N loss potential. These findings suggest that deficit irrigation can be a tool for reducing seasonal nutrient exports from St. Augustinegrass lawns so long as fertilizer inputs are moderate. Copyright © by the American Society of Agronomy, Crop Science Society of America, and Soil Science Society of America, Inc.

  8. Mitochondrial respiration deficits driven by reactive oxygen species in experimental temporal lobe epilepsy.

    Science.gov (United States)

    Rowley, Shane; Liang, Li-Ping; Fulton, Ruth; Shimizu, Takahiko; Day, Brian; Patel, Manisha

    2015-03-01

    Metabolic alterations have been implicated in the etiology of temporal lobe epilepsy (TLE), but whether or not they have a functional impact on cellular energy producing pathways (glycolysis and/or oxidative phosphorylation) is unknown. The goal of this study was to determine if alterations in cellular bioenergetics occur using real-time analysis of mitochondrial oxygen consumption and glycolytic rates in an animal model of TLE. We hypothesized that increased steady-state levels of reactive oxygen species (ROS) initiated by epileptogenic injury result in impaired mitochondrial respiration. We established methodology for assessment of bioenergetic parameters in isolated synaptosomes from the hippocampus of Sprague-Dawley rats at various times in the kainate (KA) model of TLE. Deficits in indices of mitochondrial respiration were observed at time points corresponding with the acute and chronic phases of epileptogenesis. We asked if mitochondrial bioenergetic dysfunction occurred as a result of increased mitochondrial ROS and if it could be attenuated in the KA model by pharmacologically scavenging ROS. Increased steady-state ROS in mice with forebrain-specific conditional deletion of manganese superoxide dismutase (Sod2(fl/fl)NEX(Cre/Cre)) in mice resulted in profound deficits in mitochondrial oxygen consumption. Pharmacological scavenging of ROS with a catalytic antioxidant restored mitochondrial respiration deficits in the KA model of TLE. Together, these results demonstrate that mitochondrial respiration deficits occur in experimental TLE and ROS mechanistically contribute to these deficits. Furthermore, this study provides novel methodology for assessing cellular metabolism during the entire time course of disease development. Copyright © 2015 Elsevier Inc. All rights reserved.

  9. Meta-analysis of social cognition in attention-deficit/hyperactivity disorder (ADHD): comparison with healthy controls and autistic spectrum disorder.

    Science.gov (United States)

    Bora, E; Pantelis, C

    2016-03-01

    Impairment in social cognition is an established finding in autism spectrum disorders (ASD). Emerging evidence suggests that attention-deficit/hyperactivity disorder (ADHD) might be also associated with deficits in theory of mind (ToM) and emotion recognition. However, there are inconsistent findings, and it has been debatable whether such deficits persist beyond childhood and how similar social cognitive deficits are in ADHD v. ASD. We conducted a meta-analysis of social cognition, including emotion recognition and ToM, studies in ADHD compared with healthy controls and ASD. The current meta-analysis involved 44 studies comparing ADHD (n = 1999) with healthy controls (n = 1725) and 17 studies comparing ADHD (n = 772) with ASD (n = 710). Facial and vocal emotion recognition (d = 0.40-0.44) and ToM (d = 0.43) abilities were significantly impaired in ADHD. The most robust facial emotion recognition deficits were evident in anger and fear. Social cognitive deficits were either very subtle (emotion recognition) or non-significant (ToM) in adults with ADHD. Deficits in social cognition, especially ToM, were significantly more pronounced in ASD compared with ADHD. General cognitive impairment has contributed to social cognitive deficits in ADHD. Performance of individuals with ADHD on social cognition lies intermediate between ASD and healthy controls. However, developmental trajectories of social cognition probably differ between ADHD and ASD as social cognitive deficits in ADHD might be improving with age in most individuals. There is a need for studies investigating a potential subtype of ADHD with persistent social cognitive deficits and exploring longitudinal changes in social cognition during development.

  10. Stroke caused auditory attention deficits in children

    Directory of Open Access Journals (Sweden)

    Karla Maria Ibraim da Freiria Elias

    2013-01-01

    Full Text Available OBJECTIVE: To verify the auditory selective attention in children with stroke. METHODS: Dichotic tests of binaural separation (non-verbal and consonant-vowel and binaural integration - digits and Staggered Spondaic Words Test (SSW - were applied in 13 children (7 boys, from 7 to 16 years, with unilateral stroke confirmed by neurological examination and neuroimaging. RESULTS: The attention performance showed significant differences in comparison to the control group in both kinds of tests. In the non-verbal test, identifications the ear opposite the lesion in the free recall stage was diminished and, in the following stages, a difficulty in directing attention was detected. In the consonant- vowel test, a modification in perceptual asymmetry and difficulty in focusing in the attended stages was found. In the digits and SSW tests, ipsilateral, contralateral and bilateral deficits were detected, depending on the characteristics of the lesions and demand of the task. CONCLUSION: Stroke caused auditory attention deficits when dealing with simultaneous sources of auditory information.

  11. Taxation, Fiscal Deficit and Inflation in Pakistan

    Directory of Open Access Journals (Sweden)

    Ghulam Rasool Madni

    2014-09-01

    Full Text Available Fiscal policy has more controversial debate regarding its effectiveness on different macroeconomic activities of an economy. Taxation and government expenditure are two main instruments of fiscal policy. This paper is aimed to analyze and update the effects of different instruments of fiscal policy on inflation in Pakistan economy. The data time span for this study is 1979-2013. The impact of fiscal policy on inflation is analyzed by utilizing the Bounds testing procedure and ARDL approach of co-integration which is a better estimation technique for small sample size. It is found that investment negatively and significantly affect the inflation rate. The outcomes of the study show that both types of taxes (direct and indirect are causing to increase the inflation level while fiscal deficit is also one of the reasons to increase the inflation in the country. The study proposed that government should decrease the level of expenditure to reduce the level of fiscal deficit and investment have to be promoted to decrease the inflation in the country. Furthermore, it is also suggested to decrease the level of taxation for controlling inflation.

  12. Word learning in children with vocabulary deficits.

    Science.gov (United States)

    Nash, Marysia; Donaldson, Morag L

    2005-04-01

    Word learning in 16 children with specific language impairment (SLI) was compared with that of chronological-age controls (CAC) and vocabulary-age controls (VAC), to examine the extent and nature of word-learning deficits in the children with SLI. The children were exposed to novel words in a story and an explicit teaching context. Five tasks assessed how much the children had learned about the words' phonological form and semantic properties after 6 repetitions (Time 1) and again after 12 repetitions (Time 2) of the words in each context. The SLI group performed significantly worse than the CAC group at both Time 1 and Time 2 on all measures of the words presented in both contexts. They performed similarly to the VAC group (who were on average 21/2 years younger) on Time 1 and Time 2 measures from both contexts, except for the Naming task at Time 2, on which their performance was significantly lower. These findings suggest that children with vocabulary deficits have difficulties with both phonological and semantic aspects of word learning.

  13. Musical, visual and cognitive deficits after middle cerebral artery infarction

    OpenAIRE

    Rosemann, Stephanie; Brunner, Freimuth; Kastrup, Andreas; Fahle, Manfred

    2017-01-01

    The perception of music can be impaired after a stroke. This dysfunction is called amusia and amusia patients often also show deficits in visual abilities, language, memory, learning, and attention. The current study investigated whether deficits in music perception are selective for musical input or generalize to other perceptual abilities. Additionally, we tested the hypothesis that deficits in working memory or attention account for impairments in music perception. Twenty stroke patients w...

  14. Investigación neuroquímica cerebral y aplicación preventiva para la reducción de los índices de criminalidad/Neurochemical brain research and it’s preventive application to reduce the crime statistics

    Directory of Open Access Journals (Sweden)

    Osvaldo Tieghi (Argentina

    2014-01-01

    Full Text Available Investigación neuroquímica cerebral y aplicación preventiva para la reducción de los índices de criminalidad Neurochemical brain research and it’s preventive application to reduce the crime statistics

  15. The Twin Deficits Hypothesis: An Empirical Analysis for Tanzania

    Directory of Open Access Journals (Sweden)

    Manamba Epaphra

    2017-09-01

    Full Text Available This paper examines the relationship between current account and government budget deficits in Tanzania. The paper tests the validity of the twin deficits hypothesis, using annual time series data for the 1966-2015 period. The paper is thought to be significant because the concept of the twin deficit hypothesis is fraught with controversy. Some researches support the hypothesis that there is a positive relationship between current account deficits and fiscal deficits in the economy while others do not. In this paper, the empirical tests fail to reject the twin deficits hypothesis, indicating that rising budget deficits put more strain on the current account deficits in Tanzania. Specifically, the Vector Error Correction Model results support the conventional theory of a positive relationship between fiscal and external balances, with a relatively high speed of adjustment toward the equilibrium position. This evidence is consistent with a small open economy. To address the problem that may result from this kind of relationship, appropriate policy variables for reducing budget deficits such as reduction in non-development expenditure, enhancement of domestic revenue collection and actively fight corruption and tax evasion should be adopted. The government should also target export oriented firms and encourage an import substitution industry by creating favorable business environments.

  16. Cortical Structural Abnormalities in Deficit Versus Nondeficit Schizophrenia

    Science.gov (United States)

    Fischer, Bernard A.; Keller, William R.; Arango, Celso; Pearlson, Godfrey; McMahon, Robert P.; Meyer, Walter A.; Francis, Alan; Kirkpatrick, Brian; Carpenter, William T.; Buchanan, Robert W.

    2012-01-01

    Objective To examine the structural integrity of the dorsolateral prefrontal-basal ganglia-thalamocortical circuit in people with the deficit form of schizophrenia. Method A three-dimensional structural MRI sequence was used to conduct morphometric assessments of cortical and subcortical regions in deficit and nondeficit outpatients with schizophrenia and healthy controls. Results The superior prefrontal and superior and middle temporal gyral gray matter volumes were significantly smaller in the deficit versus the nondeficit group and normal control groups. There were no significant group differences in examined subcortical structures. Conclusion People with deficit schizophrenia are characterized by selective reductions in the prefrontal and temporal cortex. PMID:22336954

  17. Emotional Response Deficits in Schizophrenia: Insights From Affective Science

    National Research Council Canada - National Science Library

    Kring, Ann M; Moran, Erin K

    2008-01-01

    ... our understanding of emotional response deficits in schizophrenia. We review naturalistic studies and elicitation studies that evoke emotion responses among participants, including emotion expression, experience, and autonomic physiology...

  18. Musical, visual and cognitive deficits after middle cerebral artery infarction

    Directory of Open Access Journals (Sweden)

    Stephanie Rosemann

    2017-03-01

    Full Text Available The perception of music can be impaired after a stroke. This dysfunction is called amusia and amusia patients often also show deficits in visual abilities, language, memory, learning, and attention. The current study investigated whether deficits in music perception are selective for musical input or generalize to other perceptual abilities. Additionally, we tested the hypothesis that deficits in working memory or attention account for impairments in music perception. Twenty stroke patients with small infarctions in the supply area of the middle cerebral artery were investigated with tests for music and visual perception, categorization, neglect, working memory and attention. Two amusia patients with selective deficits in music perception and pronounced lesions were identified. Working memory and attention deficits were highly correlated across the patient group but no correlation with musical abilities was obtained. Lesion analysis revealed that lesions in small areas of the putamen and globus pallidus were connected to a rhythm perception deficit. We conclude that neither a general perceptual deficit nor a minor domain general deficit can account for impairments in the music perception task. But we find support for the modular organization of the music perception network with brain areas specialized for musical functions as musical deficits were not correlated to any other impairment.

  19. Attention deficit-hyperactivity disorder and early-onset bipolar disorder: two facets of one entity?

    OpenAIRE

    Zepf, Florian D.

    2009-01-01

    Early-onset bipolar disorder (BD) and attention-deficithyperactivity disorder (ADHD) have recently been the subject of highly controversial debate, due to theories regarding underlying pathophysiological processes and a clinical overlap of symptoms. Epidemiological data, clinical aspect, neuroimaging, neurochemical, and genetic studies suggest that there may be a possible relationship between biological factors and clinical characteristic in the development of symptoms. However, longitudinal ...

  20. Gene-environment interaction between lead and Apolipoprotein E4 causes cognitive behavior deficits in mice.

    Science.gov (United States)

    Engstrom, Anna K; Snyder, Jessica M; Maeda, Nobuyo; Xia, Zhengui

    2017-02-07

    Alzheimer's disease (AD) is characterized by progressive cognitive decline and memory loss. Environmental factors and gene-environment interactions (GXE) may increase AD risk, accelerate cognitive decline, and impair learning and memory. However, there is currently little direct evidence supporting this hypothesis. In this study, we assessed for a GXE between lead and ApoE4 on cognitive behavior using transgenic knock-in (KI) mice that express the human Apolipoprotein E4 allele (ApoE4-KI) or Apolipoprotein E3 allele (ApoE3-KI). We exposed 8-week-old male and female ApoE3-KI and ApoE4-KI mice to 0.2% lead acetate via drinking water for 12 weeks and assessed for cognitive behavior deficits during and after the lead exposure. In addition, we exposed a second (cellular) cohort of animals to lead and assessed for changes in adult hippocampal neurogenesis as a potential underlying mechanism for lead-induced learning and memory deficits. In the behavior cohort, we found that lead reduced contextual fear memory in all animals; however, this decrease was greatest and statistically significant only in lead-treated ApoE4-KI females. Similarly, only lead-treated ApoE4-KI females exhibited a significant decrease in spontaneous alternation in the T-maze. Furthermore, all lead-treated animals developed persistent spatial working memory deficits in the novel object location test, and this deficit manifested earlier in ApoE4-KI mice, with female ApoE4-KI mice exhibiting the earliest deficit onset. In the cellular cohort, we observed that the maturation, differentiation, and dendritic development of adult-born neurons in the hippocampus was selectively impaired in lead-treated female ApoE4-KI mice. These data suggest that GXE between ApoE4 and lead exposure may contribute to cognitive impairment and that impaired adult hippocampal neurogenesis may contribute to these deficits in cognitive behavior. Together, these data suggest a role for GXE and sex differences in AD risk.

  1. Energy system contributions and determinants of performance in sprint cross-country skiing

    DEFF Research Database (Denmark)

    Andersson, E; Björklund, G; Holmberg, H-C

    2017-01-01

    To improve current understanding of energy contributions and determinants of sprint-skiing performance, 11 well-trained male cross-country skiers were tested in the laboratory for VO2max , submaximal gross efficiency (GE), maximal roller skiing velocity, and sprint time-trial (STT) performance...... contribution was 18 ± 5%, with an accumulated O2 deficit of 45 ± 13 mL/kg. Block-wise multiple regression revealed that VO2 , O2 deficit, and GE explained 30%, 15%, and 53% of the variance in STT time, respectively (all P skiing...

  2. Social skills deficits and their association with Internet addiction and activities in adolescents with attention-deficit/hyperactivity disorder

    OpenAIRE

    Chou, Wen-Jiun; Huang, Mei-Feng; Chang, Yu-Ping; Chen, Yu-Min,; HU, HUEI-FAN; Yen, Cheng-Fang

    2017-01-01

    Background and aims The aims of this study were to examine the association between social skills deficits and Internet addiction and activities in adolescents with attention-deficit/hyperactivity disorder (ADHD) as well as the moderators for this association. Methods A total of 300 adolescents, aged between 11 and 18 years, who had been diagnosed with ADHD participated in this study. Their Internet addiction levels, social skills deficits, ADHD, parental characteristics, and comorbidities wer...

  3. Neurochemical and structural markers in the brain predicting best choice-of-treatment in patients with schizophrenia - The Pan European Collaboration on Antipsychotic Naïve Schizophrenia II (PECANS II) study

    DEFF Research Database (Denmark)

    Jessen, Kasper; Bojesen, Kirsten Borup; Sigvard, Anne Mette

    the progressive loss of brain tissue and social functions seen in many patients. Aim of PECANS II: To test if persistently high levels of glutamate and loss of brain tissue and social functions characterize a subgroup of patients with poor treatment response, while dopaminergic disturbances characterize another...... as markers for best-choice-of-treatment. Further, the results can pave the way for the development of new antipsychotic medication modulating glutamatergic disturbances and lead to better prevention strategies for the progressive loss of brain tissue and social functions in a treatment resistant subgroup...... disturbances with positron emission tomography (PET) scanning, and loss of brain tissue with analysis of a structural MR-scanning revealing loss of cortical thickness and surface area. Neurochemical and structural disturbances are compared with treatment response and level of function as measured by various...

  4. Inhibiting corticosterone synthesis during fear memory formation exacerbates cued fear extinction memory deficits within the single prolonged stress model.

    Science.gov (United States)

    Keller, Samantha M; Schreiber, William B; Stanfield, Briana R; Knox, Dayan

    2015-01-01

    Using the single prolonged stress (SPS) animal model of post-traumatic stress disorder (PTSD), previous studies suggest that enhanced glucocorticoid receptor (GR) expression leads to cued fear extinction retention deficits. However, it is unknown how the endogenous ligand of GRs, corticosterone (CORT), may contribute to extinction retention deficits in the SPS model. Given that CORT synthesis during fear learning is critical for fear memory consolidation and SPS enhances GR expression, CORT synthesis during fear memory formation could strengthen fear memory in SPS rats by enhancing GR activation during fear learning. In turn, this could lead to cued fear extinction retention deficits. We tested the hypothesis that CORT synthesis during fear learning leads to cued fear extinction retention deficits in SPS rats by administering the CORT synthesis inhibitor metyrapone to SPS and control rats prior to fear conditioning, and observed the effect this had on extinction memory. Inhibiting CORT synthesis during fear memory formation in control rats tended to decrease cued freezing, though this effect never reached statistical significance. Contrary to our hypothesis, inhibiting CORT synthesis during fear memory formation disrupted extinction retention in SPS rats. This finding suggests that even though SPS exposure leads to cued fear extinction memory deficits, CORT synthesis during fear memory formation enhances extinction retention in SPS rats. This suggests that stress-induced CORT synthesis in previously stressed rats can be beneficial. Copyright © 2015 Elsevier B.V. All rights reserved.

  5. Frontal deficits differentiate progressive supranuclear palsy from Parkinson's disease.

    Science.gov (United States)

    Lee, Young-Eun C; Williams, David R; Anderson, Jacqueline F I

    2016-03-01

    The clinical differentiation of progressive supranuclear palsy from Parkinson's disease can be challenging, due to overlapping clinical features and a lack of diagnostic markers. Abnormalities in cognitive function form part of the clinical spectrums of these diseases and distinctive cognitive profiles may be helpful in differentiating these diseases in the diagnostic period. A comprehensive neuropsychological test battery was administered to 12 patients with clinically diagnosed progressive supranuclear palsy and 12 patients with Parkinson's disease matched for age and disease duration. Effect size (Cohen's d) was calculated for cognitive tests that were significantly different between groups. Patients with progressive supranuclear palsy performed significantly worse than those with Parkinson's disease on measures of processing speed, verbal fluency, planning, verbal abstract reasoning, verbal memory, and made more perseverative responses on a set shifting task. Measures of executive function, manual dexterity and processing speed were most diagnostically useful (Cohen's d > 2.0) in differentiating between progressive supranuclear palsy and Parkinson's disease. These findings suggest that more severe and prominent 'frontal' cognitive deficits in patients with progressive parkinsonism would be helpful in predicting progressive supranuclear palsy rather than Parkinson's disease and these findings may contribute to the development of diagnostic criteria. © 2014 The British Psychological Society.

  6. [Heritability and genetic comorbidity of attention deficit disorder with hyperactivity].

    Science.gov (United States)

    Puddu, Giannina; Rothhammer, Paula; Carrasco, Ximena; Aboitiz, Francisco; Rothhammer, Francisco

    2017-03-01

    This review aims to summarize information about the genetic etiology of attention deficit disorder with hyperactivity (ADHD), with particular reference to the contributions of our research group. We also discuss the genetic comorbidity estimated from genome-wide single nucleotide polymorphisms (SNP´s) between ADHD and major psychiatric disorders such as schizophrenia (E), major depressive disorder (MDD), bipolar disorder (BD) and autism spectrum disorders (ASD). A high genetic comorbidity was found between E and BD (46%), a moderate comorbidity between MDD and E, MDD and BD and MDD and ADHD (18%, 22% and 10% respectively) and a low comorbidity between E and ASD (2.5%). Furthermore, we show evidence concerning the genetic determination of psychiatric diseases, which is significantly lower when it is estimated from genome-wide SNP´s rather than using traditional quantitative genetic methodology (ADHD = E = 23%, BD = 25%, MDD = 21% and ASD = 17%). From an evolutionary perspective, we suggest that behavioral traits such as hyperactivity, inattention and impulsivity, which play a role in ADHD and perhaps also other hereditary traits which are part of major psychiatric disorders, could have had a high adaptive value during the early stages of the evolution of Homo sapiens. However, they became progressively less adaptive and definitively disadvantageous, to the extreme that they are involved in frequently diagnosed major psychiatric disorders.

  7. ADHDgene: a genetic database for attention deficit hyperactivity disorder

    Science.gov (United States)

    Zhang, Liuyan; Chang, Suhua; Li, Zhao; Zhang, Kunlin; Du, Yang; Ott, Jurg; Wang, Jing

    2012-01-01

    With a worldwide prevalence of ∼5%, attention deficit hyperactivity disorder (ADHD) has become one of the most common psychiatric disorders. The polygenetic nature of ADHD indicates that multiple genes jointly contribute to the development of this complex disease. Studies aiming to explore genetic susceptibility of ADHD have been increasing in recent years. There is a growing need to integrate the genetic data from various genetic studies to provide a comprehensive data set and uniform access for convenience of in-depth data mining. So far, there has been no such effort for ADHD. To address the genetic complexity of ADHD, we developed the ADHDgene database by integrating ADHD-related genetic factors by profound literature reading. Based on the data from the literature, extended functional analysis, including linkage disequilibrium analysis, pathway-based analysis and gene mapping were performed to provide new insights into genetic causes of ADHD. Moreover, powerful search tools and a graphical browser were developed to facilitate the navigation of the data and data connections. As the first genetic database for ADHD, ADHDgene aims to provide researchers with a central genetic resource and analysis platform for ADHD and is freely available at http://adhd.psych.ac.cn/. PMID:22080511

  8. The intergenerational multiple deficit model and the case of dyslexia.

    Science.gov (United States)

    van Bergen, Elsje; van der Leij, Aryan; de Jong, Peter F

    2014-01-01

    Which children go on to develop dyslexia? Since dyslexia has a multifactorial etiology, this question can be restated as: what are the factors that put children at high risk for developing dyslexia? It is argued that a useful theoretical framework to address this question is Pennington's (2006) multiple deficit model (MDM). This model replaces models that attribute dyslexia to a single underlying cause. Subsequently, the generalist genes hypothesis for learning (dis)abilities (Plomin and Kovas, 2005) is described and integrated with the MDM. Next, findings are presented from a longitudinal study with children at family risk for dyslexia. Such studies can contribute to testing and specifying the MDM. In this study, risk factors at both the child and family level were investigated. This led to the proposed intergenerational MDM, in which both parents confer liability via intertwined genetic and environmental pathways. Future scientific directions are discussed to investigate parent-offspring resemblance and transmission patterns, which will shed new light on disorder etiology.

  9. The intergenerational multiple deficit model and the case of dyslexia

    Directory of Open Access Journals (Sweden)

    Elsje evan Bergen

    2014-06-01

    Full Text Available Which children go on to develop dyslexia? Since dyslexia has a multifactorial aetiology, this question can be restated as: What are the factors that put children at high risk for developing dyslexia? It is argued that a useful theoretical framework to address this question is Pennington’s (2006 multiple deficit model (MDM. This model replaces models that attribute dyslexia to a single underlying cause. Subsequently, the generalist genes hypothesis for learning (disabilities (Plomin & Kovas, 2005 is described and integrated with the MDM. Finally, findings are presented from a longitudinal study with children at family risk for dyslexia. Such studies can contribute to testing and specifying the MDM. In this study, risk factors at both the child and family level were investigated. This led to the proposed intergenerational MDM, in which both parents confer liability via intertwined genetic and environmental pathways. Future scientific directions are discussed to investigate parent-offspring resemblance and transmission patterns, which will shed new light on disorder aetiology.

  10. The intergenerational multiple deficit model and the case of dyslexia

    Science.gov (United States)

    van Bergen, Elsje; van der Leij, Aryan; de Jong, Peter F.

    2014-01-01

    Which children go on to develop dyslexia? Since dyslexia has a multifactorial etiology, this question can be restated as: what are the factors that put children at high risk for developing dyslexia? It is argued that a useful theoretical framework to address this question is Pennington’s (2006) multiple deficit model (MDM). This model replaces models that attribute dyslexia to a single underlying cause. Subsequently, the generalist genes hypothesis for learning (dis)abilities (Plomin and Kovas, 2005) is described and integrated with the MDM. Next, findings are presented from a longitudinal study with children at family risk for dyslexia. Such studies can contribute to testing and specifying the MDM. In this study, risk factors at both the child and family level were investigated. This led to the proposed intergenerational MDM, in which both parents confer liability via intertwined genetic and environmental pathways. Future scientific directions are discussed to investigate parent-offspring resemblance and transmission patterns, which will shed new light on disorder etiology. PMID:24920944

  11. Attention-deficit/hyperactivity disorder (ADHD)

    DEFF Research Database (Denmark)

    Dalsgaard, S.

    2013-01-01

    The proposed revision of the diagnostic criteria in DSM-5 for attention-deficit/hyperactivity disorder (ADHD) will not fundamentally change the concept of ADHD. This is mainly due to the fact that, DSM-5 will retain the exact DSM-IV wording of all 18 symptoms, but will add new examples that make...... the criteria more appropriate for children, adolescents and adults. The age of onset will also be changed from 7 to 12 years, the subtyping of the disorder will change, and pervasive developmental disorders will no longer be an exclusion criterion. Although the main concept is unchanged, the suggested changes...... will most likely increase the prevalence of ADHD, especially in adults and adolescents, but maybe also in children. The added examples will also result in necessary revisions and new validations of rating scales and diagnostic interviews. This review will examine each of the proposed DSM-5 changes...

  12. Nonlinear spelling in graphemic buffer deficit.

    Science.gov (United States)

    Schubert, Teresa; Nickels, Lyndsey

    2015-01-01

    In this paper, we describe a case of nonlinear spelling and its implications for theories of the graphemic buffer. C.T.J., an individual with an acquired deficit of the graphemic buffer, often wrote the letters of his responses in a nonlinear temporal order when writing to dictation. The spatial ordering of the letters was maintained: Letters in the later positions of the words were written towards the right side of the response, even when written before letters in earlier positions. This unusual phenomenon has been briefly reported in three prior cases but this study provides the most detailed analysis of the phenomenon to date. We specifically contend that the decoupling of the temporal and spatial aspects of spelling is difficult to reconcile with competitive queuing accounts of the graphemic buffer.

  13. Genetic Basis of Attention Deficit Hyperactivity Disorder

    Directory of Open Access Journals (Sweden)

    Nihal Yurteri

    2011-01-01

    Full Text Available Attention Deficit Hyperactivity Disorder (ADHD is one of the most common neuropsychiatric disorders of childhood. Due to studies reporting that the effects of ADHD diagnosis on functioning may last throughout life, this disorder, which has great importance for child and adolescent psychiatry, started to attract greater attention recently in terms of adult psychiatry. A review, evaluating the results of studies conducted on the genetic basis of ADHD, which started to attract increasing attention both in our country and the world, was thought to help clinicians working in this field. PubMed and Turkish Psychiatry Index online search engines were screened using “attention deficit hyperactivity disorder”, “ADHD”, “genetics” as key words. The data obtained were combined with information gleaned from several textbooks. Based on previous studies, it could easily be concluded that ADHD is one of the most common heritable psychiatric disorder with distinguished genetic features. Despite its importance for diagnosis and treatment, the etiology of ADHD is still not clear and the disorder seems to be a complex problem arising from the effects of both genetic and environmental factors. Although previous studies revealed that ADHD displayed familial and hereditary transmission, stable patterns of Mendelian inheritance could not be discriminated by evaluation of pedigrees. Therefore, many studies have been conducted on the molecular genetic basis of ADHD recently. The previous studies did not report consistent results in identification of the genes responsible for ADHD which has been partially linked to heterogeneity of the disorder. Grouping relevant patients according to comorbidities and persistence in adolescence rather than DSM-IV subtypes could be an important alternative method for overcoming this limitation in the research studies.

  14. Oculomotor Deficits after Chemotherapy in Childhood.

    Directory of Open Access Journals (Sweden)

    Einar-Jón Einarsson

    Full Text Available Advances in the diagnosis and treatment of pediatric malignancies have substantially increased the number of childhood cancer survivors. However, reports suggest that some of the chemotherapy agents used for treatment can cross the blood brain barrier which may lead to a host of neurological symptoms including oculomotor dysfunction. Whether chemotherapy at young age causes oculomotor dysfunction later in life is unknown. Oculomotor performance was assessed with traditional and novel methods in 23 adults (mean age 25.3 years, treatment age 10.2 years treated with chemotherapy for a solid malignant tumor not affecting the central nervous system. Their results were compared to those from 25 healthy, age-matched controls (mean age 25.1 years. Correlation analysis was performed between the subjective symptoms reported by the chemotherapy treated subjects (CTS and oculomotor performance. In CTS, the temporal control of the smooth pursuit velocity (velocity accuracy was markedly poorer (p<0.001 and the saccades had disproportionally shorter amplitude than normal for the associated saccade peak velocity (main sequence (p = 0.004, whereas smooth pursuit and saccade onset times were shorter (p = 0.004 in CTS compared with controls. The CTS treated before 12 years of age manifested more severe oculomotor deficits. CTS frequently reported subjective symptoms of visual disturbances (70%, unsteadiness, light-headedness and that things around them were spinning or moving (87%. Several subjective symptoms were significantly related to deficits in oculomotor performance. To conclude, chemotherapy in childhood or adolescence can result in severe oculomotor dysfunctions in adulthood. The revealed oculomotor dysfunctions were significantly related to the subjects' self-perception of visual disturbances, dizziness, light-headedness and sensing unsteadiness. Assessments of oculomotor function may, thus, offer an objective method to track and rate the level of

  15. Attention-deficit-hyperactivity disorder: an update.

    Science.gov (United States)

    Dopheide, Julie A; Pliszka, Steven R

    2009-06-01

    Attention-deficit-hyperactivity disorder (ADHD) is a common neuropsychiatric disorder that impairs social, academic, and occupational functioning in children, adolescents, and adults. In patients with ADHD, neurobiologic research has shown a lack of connectivity in key brain regions, inhibitory control deficits, delayed brain maturation, and noradrenergic and dopaminergic dysfunction in multiple brain regions. The prevalence of this disorder in the United States is 6-9% in youth (i.e., children and adolescents) and 3-5% in adults. Prevalence rates for youth are similar worldwide. Children with ADHD are at greater risk than children without ADHD for substance abuse and delinquency whether or not they receive drug therapy; however, early treatment with psychoeducation as well as drug therapy and/or behavioral intervention may decrease negative outcomes of ADHD, including the rate of conduct disorder and adult antisocial personality disorder. Drug therapy is effective for all age groups, even preschoolers, and for late-onset ADHD in adults. Stimulants, such as methylphenidate and amphetamine, are the most effective therapy and have a good safety profile; although recent concerns of sudden unexplained death, psychiatric adverse effects, and growth effects have prompted the introduction of other therapies. Atomoxetine, a nonstimulant, has no abuse potential, causes less insomnia than stimulants, and poses minimal risk of growth effects. Other drug options include clonidine and guanfacine, but both can cause bradycardia and sedation. Polyunsaturated fatty acids (fish oil), acetyl-L-carnitine, and iron supplements (for youth with low ferritin levels) show promise in improving ADHD symptoms. As long-term studies show that at least 50% of youth are nonadherent with their drug therapy as prescribed over a 1-year period, long-acting formulations (administered once/day) may improve adherence. Comorbid conditions are common in patients with ADHD, but this patient population can

  16. Tactile morphagnosia secondary to spatial deficits.

    Science.gov (United States)

    Saetti, M C; De Renzi, E; Comper, M

    1999-08-01

    A 73-year old man showed visual and tactile agnosia following bilateral haemorrhagic stroke. Tactile agnosia was present in both hands, as shown by his impaired recognition of objects, geometrical shapes, letters and nonsense shapes. Basic somatosensory functions and the appreciation of substance qualities (hylognosis) were preserved. The patient's inability to identify the stimulus shape (morphagnosia) was associated with a striking impairment in detecting the orientation of a line or a rod in two- and three-dimensional space. This spatial deficit was thought to underlie morphagnosia, since in the tactile modality form recognition is built upon the integration of the successive changes of orientation in space made by the hand as it explores the stimulus. Indirect support for this hypothesis was provided by the location of the lesions, which could not account for the severe impairment of both hands. Only those located in the right hemisphere encroached upon the posterior parietal cortex, which is the region assumed to be specialised in shape recognition. The left hemisphere damage spared the corresponding area and could not, therefore, be held responsible for the right hand tactile agnosia. We submit that tactile agnosia can result from the disruption of two discrete mechanisms and has different features. It may arise from a parietal lesion damaging the high level processing of somatosensory information that culminates in the structured description of the object. In this case, tactile recognition is impaired in the hand contralateral to the side of the lesion. Alternatively, it may be caused by a profound derangement of spatial skills, particularly those involved in detecting the orientation in space of lines, segments and complex patterns. This deficit results in morphagnosia, which affects both hands to the same degree.

  17. Stigmatization in teachers towards adults with attention deficit hyperactivity disorder.

    Science.gov (United States)

    Fuermaier, Anselm Bm; Tucha, Lara; Mueller, Anna K; Koerts, Janneke; Hauser, Joachim; Lange, Klaus W; Tucha, Oliver

    2014-01-14

    Attention deficit hyperactivity disorder (ADHD) is understood as a developmental disorder which shares common characteristics between childhood, adolescence and adulthood. However, ADHD is widely associated with misconceptions and misbeliefs which can lead to stigmatization. Teachers have an important role for the individual development as they accompany students for a long period of time. The aim of the present study was to explore stigmatizing attitudes in teachers towards adults with ADHD, thereby focusing on the developmental trajectory of the condition. Furthermore, it was aimed to identify factors contributing to prevention and intervention of stigmatization in ADHD. Stigma responses of 170 teachers and 170 comparison participants were measured and compared with a recently developed tool for the assessment of stigmatization towards adults with ADHD. Furthermore, the contribution of knowledge about ADHD and the frequency of contact with adults with ADHD to stigmatization were explored. Teachers showed significantly less stigmatizing attitudes than comparison participants in various dimensions, including Reliability and Social Functioning, Malingering and Misuse of Medication and the total scale. With regard to teachers, frequency of contact with adults with ADHD was not related to stigma. However, knowledge about the disorder was negatively correlated with stigma in teachers, indicating lower expressed stigma with increasing knowledge about adult ADHD. Teachers demonstrated more sensitized attitudes towards stigma in adults with ADHD than comparison participants. Since the present results indicate that knowledge about ADHD increase the sensitivity towards the disorder, special education programs for the community may have the potential to reduce stigmatization towards adults with ADHD. Possibilities for intervention strategies of stigmatization in educational settings were discussed.

  18. Social perception deficits, cognitive distortions, and empathy deficits in sex offenders: a brief review.

    Science.gov (United States)

    Blake, Emily; Gannon, Theresa

    2008-01-01

    This literature review examines the differences between sex offenders and nonoffenders with regard to social perception skills, cognitive distortions, and empathy skills in order to investigate sex offenders' cognition. The literature on cognitive distortions is discussed, with reference to the confusion surrounding its definition, and the debate between cognitive distortions as offense-supportive beliefs or justifications is examined. In terms of social perception, particular reference is made to sex offenders' misinterpretations of women's social cues and the source of this deficit. The authors discuss possibilities for this deficit, including offense-supportive beliefs that are driven by underlying implicit theories or schemata held by offenders. The concept of empathy and its relation to both social perception skills and cognitive distortions is discussed, and the integration of these factors is represented in a new model.

  19. Exploring the nature of facial affect processing deficits in schizophrenia.

    NARCIS (Netherlands)

    Wout, M. van 't; Aleman, A.; Kessels, R.P.C.; Cahn, W.; Haan, E.H.F. de; Kahn, R.S.

    2007-01-01

    Schizophrenia has been associated with deficits in facial affect processing, especially negative emotions. However, the exact nature of the deficit remains unclear. The aim of the present study was to investigate whether schizophrenia patients have problems in automatic allocation of attention as

  20. Effect of progressive water deficit stress on proline accumulation and ...

    African Journals Online (AJOL)

    Water deficit stress is one of the important factors limiting chickpea production in arid and semi-arid regions of West Asia and North Africa. When water deficit stress is imposed, different molecular and biochemical responses take place. This study was carried out to investigate proline accumulation and protein profiles of ...

  1. Fiscal Deficits and Inflation in Nigeria | Ozurumba | Journal of ...

    African Journals Online (AJOL)

    This paper examines the causal relationship between inflation and fiscal deficits in Nigeria, covering the period 1970-2009. This was carried out by way of developing an estimation model of inflation and fiscal deficit, with a view to testing causes and effects as well as the relationship between them. The estimation technique ...

  2. Psychosocial and Adaptive Deficits Associated with Learning Disability Subtypes

    Science.gov (United States)

    Backenson, Erica M.; Holland, Sara C.; Kubas, Hanna A.; Fitzer, Kim R.; Wilcox, Gabrielle; Carmichael, Jessica A.; Fraccaro, Rebecca L.; Smith, Amanda D.; Macoun, Sarah J.; Harrison, Gina L.; Hale, James B.

    2015-01-01

    Children with specific learning disabilities (SLD) have deficits in the basic psychological processes that interfere with learning and academic achievement, and for some SLD subtypes, these deficits can also lead to emotional and/or behavior problems. This study examined psychosocial functioning in 123 students, aged 6 to 11, who underwent…

  3. Overcoming Executive Function Deficits with Students with ADHD

    Science.gov (United States)

    Johnson, Joseph; Reid, Robert

    2011-01-01

    Academic problems are common among students with attention deficit hyperactivity disorder (ADHD). One reason for academic problems is the difficulties in executive functions (EF) that are necessary for complex goal-oriented behaviors. Students with ADHD often exhibit EF deficits and as a result have difficulties with tasks that require planning,…

  4. Neuropsychological Treatment of Attention Deficit Disorder in Infancy

    Science.gov (United States)

    Solovieva, Yulia; Quintanar, Luis

    2017-01-01

    The syndrome of attention deficit disorder is one of the most frequent pictures of disabilities in pre-scholars. The present study analyses the results of fulfillment of tasks for mechanisms of control and spatial functions. 14 pre-scholars with attention deficit disorder took part in the study. The neuropsychological evaluation was applied before…

  5. Studies on water deficits on apical development and panicle ...

    African Journals Online (AJOL)

    Leaf primordium production was severely inhibited by periods of water deficit, with apparent cessation occurring around a dawn water potential of -1.0 MPa. Panicle initiation was delayed according to the duration of water deficit and the period of cessation of leaf primordium production. The duration of growth stages two ...

  6. Estimating runoff and soil moisture deficit in guinea savannah region ...

    African Journals Online (AJOL)

    Estimating runoff and soil moisture deficit in guinea savannah region of Nigeria using water balance method. ... The estimation ofrunoff and soil moisture deficit in Guinea Savannah region using semi arid model based on soil water balance technique (SAMBA) was carried out. The input to the SAMBA model are daily rainfall ...

  7. Democracy in the Arab World: Explaining the Deficit | IDRC ...

    International Development Research Centre (IDRC) Digital Library (Canada)

    2010-09-10

    Sep 10, 2010 ... Despite notable socio-economic development in the Arab region, a deficit in democracy and political rights has continued to prevail. This book examines the major reasons underlying the persistence of this democracy deficit over the past decades and touches on the prospect for deepening the process of ...

  8. Test Review: Barkley Deficits in Executive Functioning Scale (BDEFS)

    Science.gov (United States)

    Allee-Smith, Paula J.; Winters, Rebecca R.; Drake, Amanda; Joslin, Amanda K.

    2013-01-01

    The Barkley Deficits in Executive Functioning Scale (BDEFS), authored by Russell A. Barkley and published by Guilford in 2011, is an individually administered assessment tool that may be used to evaluate adults ages 18 to 81. The purpose of this measure is to screen those who may be experiencing executive functioning (EF) deficits in…

  9. Dietary Cholesterol Protects Anesthesia-Induced Cognitive Deficits ...

    African Journals Online (AJOL)

    4. Hohsfield LA, Ehrlich D, Humpel C. Cholesterol diet counteracts repeated anesthesia/infusion-induced cognitive deficits in male Brown Norway rats. Neurobiol Learn Mem 2013; 106: 154-62. 5. Voikar V, Rauvala H, Ikonen E. Cognitive deficit and development of motor impairment in a mouse model of Niemann-Pick type ...

  10. The Deficit and the Federal Budget. 1983 National Issues Forum.

    Science.gov (United States)

    Melville, Keith, Ed.

    Although designed for participants in the National Issues Forum, this booklet, which describes the impact of the federal deficit and the federal budget process, is also useful for secondary school social studies. The six sections begin with an introduction describing why the deficit grows yearly and why it is difficult for Congress to stop its…

  11. Pragmatic Deficits and Social Impairment in Children with ADHD

    Science.gov (United States)

    Staikova, Ekaterina; Gomes, Hilary; Tartter, Vivien; McCabe, Allyssa; Halperin, Jeffrey M.

    2013-01-01

    Background: Impaired social functioning has been well documented in individuals with attention-deficit/hyperactivity disorder (ADHD). Existing treatments for ADHD are effective for managing core symptoms, but have limited effectiveness at improving social skills, suggesting that social deficits in ADHD may not be directly related to core symptoms…

  12. Auditory Temporal Processing as a Specific Deficit among Dyslexic Readers

    Science.gov (United States)

    Fostick, Leah; Bar-El, Sharona; Ram-Tsur, Ronit

    2012-01-01

    The present study focuses on examining the hypothesis that auditory temporal perception deficit is a basic cause for reading disabilities among dyslexics. This hypothesis maintains that reading impairment is caused by a fundamental perceptual deficit in processing rapid auditory or visual stimuli. Since the auditory perception involves a number of…

  13. Nigeria's Fiscal Deficits: A History of its Colonial Foundations, 1899 ...

    African Journals Online (AJOL)

    This paper shows that deficit financing of public expenditure by the Nigerian government is however not a recent issue and that it can be traced to the formative years of Nigeria's public finance in the colonial period. The paper however argues that unlike the current practice, deficit financing was driven more in the colonial ...

  14. How specific are executive functioning deficits in attention deficit hyperactivity disorder and autism?

    OpenAIRE

    Geurts, H.M.; Verté, S.; Oosterlaan, J.; Roeyers, M.; Sergeant, J. A.

    2004-01-01

    Background: The objective of this study is to identify intact and deficient cognitive processes in children with attention deficit hyperactivity disorder (ADHD) and children with high functioning autism (HFA). Method: Three rigorously diagnosed groups of children aged between 6 and 12 years (54 ADHD, 41 HFA, and 41 normal controls) were tested on a wide range of tasks related to five major domains of executive functioning (EF): inhibition, visual working memory, planning, cognitive flexibilit...

  15. Attentional set-shifting deficit in Parkinson's disease is associated with prefrontal dysfunction: an FDG-PET study.

    Directory of Open Access Journals (Sweden)

    Yoichi Sawada

    Full Text Available The attentional set-shifting deficit that has been observed in Parkinson's disease (PD has long been considered neuropsychological evidence of the involvement of meso-prefrontal and prefrontal-striatal circuits in cognitive flexibility. However, recent studies have suggested that non-dopaminergic, posterior cortical pathologies may also contribute to this deficit. Although several neuroimaging studies have addressed this issue, the results of these studies were confounded by the use of tasks that required other cognitive processes in addition to set-shifting, such as rule learning and working memory. In this study, we attempted to identify the neural correlates of the attentional set-shifting deficit in PD using a compound letter task and 18F-fluoro-deoxy-glucose (FDG positron emission tomography during rest. Shift cost, which is a measure of attentional set-shifting ability, was significantly correlated with hypometabolism in the right dorsolateral prefrontal cortex, including the putative human frontal eye field. Our results provide direct evidence that dysfunction in the dorsolateral prefrontal cortex makes a primary contribution to the attentional set-shifting deficit that has been observed in PD patients.

  16. Gray matter changes in patients with deficit schizophrenia and non-deficit schizophrenia.

    Science.gov (United States)

    Özdemir, Halil İbrahim; Eker, Mehmet Çağdaş; Zengin, Burçak; Yılmaz, Dinçer Akaydın; İşman Haznedaro