Amoxapine is used to treat depression. Amoxapine is in a class of medications called tricyclic antidepressants (TCAs). It works by increasing the amounts of certain natural substances in the brain that are ...
Full Text Available D00228 Drug Amoxapine (JP16/USP/INN); Asendin (TN) C17H16ClN3O 313.0982 313.7814 D0...28 Amoxapine (JP16/USP/INN) CAS: 14028-44-5 PubChem: 7847295 DrugBank: DB00543 LigandBox: D00228 NIKKAJI: J3
Dalkara, T; Saederup, E; Squires, R F; Krnjevic, K
Twelve substances which appear to be GABA antagonists, judging by their ability to reverse the inhibitory effect of GABA on 35S-TBPS binding to rat brain membranes, were tested iontophoretically on population spikes in the rat hippocampus. Eight of them, including seven which completely reversed the inhibitory action of GABA on 35S-TBPS binding, caused a marked enhancement of population spikes, with slow onset and long duration and they antagonized the inhibition of population spikes by GABA. These effects were similar to those produced by bicuculline. Electrophysiologically, the most potent of the "complete reversers" were bathophenanthroline disulfonate and brucine. In vitro, amoxapine and brucine most effectively reversed the inhibitory action of GABA on 35S-TBPS binding. Of the five substances which only partly reversed the inhibitory effect of GABA on 35S-TBPS binding, four depressed the population spikes and potentiated the inhibitory action of GABA. The fifth "partial reverser", pipazethate, potently increased the population spikes, like the "complete reversers". Although other interpretations are possible the results are consistent with the existence of several GABA-A receptor types in brain, only some of which are blocked by certain partial reversers. PMID:2874465
Yaman, Ayhan; Kendirli, Tanıl; Ödek, Çağlar; Yıldız, Caner; Beğde, Fırat; Erkol, Hatice; İnce, Erdal
Neuroleptic malignant syndrome (NMS) is a rare but potentially fatal complication of treatment with antipsychotic medication. NMS has also been associated with non-neuroleptic agents that block central dopamine pathways, such as metoclopramide, amoxapine and lithium. Metoclopromide has antidopaminergic properties and is a rare but well-recognized perpetrator in the development of NMS. NMS has a constellation of signs and symptoms, including hyperthermia, muscle rigidity, autonomic instability, tachycardia, tachypnea, diaphoresis, hypertension and altered mental status. We present a 2-year-old girl who developed neuroleptic malignant syndrome after metoclopromide therapy. High-dose metoclopromide was given to our patient, and it is very likely that she was dehydrated while using metoclopromide, as she developed NMS two hours after treatment. The patient was discharged on the sixth day after admission to our hospital, having been cured. In summary, NMS developed in this patient very soon after metoclopromide treatment. NMS is a life-threatening emergency; if not recognized, or left untreated, it may be fatal. Therefore, early recognition of the developing signs and symptoms, along with a thorough medical history, is of great importance.
Full Text Available Various antidepressants are commonly used for the treatment of depression and several other neuropsychiatric disorders. In addition to their primary effects on serotonergic or noradrenergic neurotransmitter systems, antidepressants have been shown to interact with several receptors and ion channels. However, the molecular mechanisms that underlie the effects of antidepressants have not yet been sufficiently clarified. G protein-activated inwardly rectifying K(+ (GIRK, Kir3 channels play an important role in regulating neuronal excitability and heart rate, and GIRK channel modulation has been suggested to have therapeutic potential for several neuropsychiatric disorders and cardiac arrhythmias. In the present study, we investigated the effects of various classes of antidepressants on GIRK channels using the Xenopus oocyte expression assay. In oocytes injected with mRNA for GIRK1/GIRK2 or GIRK1/GIRK4 subunits, extracellular application of sertraline, duloxetine, and amoxapine effectively reduced GIRK currents, whereas nefazodone, venlafaxine, mianserin, and mirtazapine weakly inhibited GIRK currents even at toxic levels. The inhibitory effects were concentration-dependent, with various degrees of potency and effectiveness. Furthermore, the effects of sertraline were voltage-independent and time-independent during each voltage pulse, whereas the effects of duloxetine were voltage-dependent with weaker inhibition with negative membrane potentials and time-dependent with a gradual decrease in each voltage pulse. However, Kir2.1 channels were insensitive to all of the drugs. Moreover, the GIRK currents induced by ethanol were inhibited by sertraline but not by intracellularly applied sertraline. The present results suggest that GIRK channel inhibition may reveal a novel characteristic of the commonly used antidepressants, particularly sertraline, and contributes to some of the therapeutic effects and adverse effects.