Blier P, de Montigny C, Chaput Y
Neuroscience Research Center, Montreal, Quebec, Canada.
J Clin Psychopharmacol. 1987 Dec;7(6 Suppl):24S-35S.
Results of electrophysiological single-cell recording studies suggest that most, if not all, types of antidepressant treatments increase 5-hydroxytryptamine (5-HT) neurotransmission. Tricyclic antidepressants, electroconvulsive shock treatment, mianserin, adinazolam, and possibly sleep deprivation may exert their therapeutic effect through sensitization of postsynaptic neurons to 5-HT. Serotonin reuptake blockers may relieve depression through an increased efficacy of the presynaptic element resulting from a desensitization of somatodendritic and terminal 5-HT autoreceptors. Similarly, monoamine oxidase inhibitors may act by increasing the efficacy of 5-HT neurons. Intensification of 5-HT function appears to be a common denominator to antidepressant treatments; however, evidence suggests that this modification may only be a link in a chain of events leading to an antidepressant response.
电生理单细胞记录研究结果表明,大多数(即便不是全部)类型的抗抑郁治疗都会增强5-羟色胺(5-HT)神经传递。三环类抗抑郁药、电休克治疗、米安色林、阿地唑仑,以及可能还有睡眠剥夺,可能通过使突触后神经元对5-HT敏感化来发挥其治疗作用。血清素再摄取阻滞剂可能通过躯体树突和终末5-HT自身受体脱敏导致突触前元件效能增加来缓解抑郁。同样,单胺氧化酶抑制剂可能通过增强5-HT神经元的效能起作用。增强5-HT功能似乎是抗抑郁治疗的一个共同特征;然而,有证据表明这种改变可能只是导致抗抑郁反应的一系列事件中的一个环节。