Lerer B
Biol Psychiatry. 1984 Mar;19(3):361-83.
Neurochemical effects of electroconvulsive shock (ECS) in three neurotransmitter-receptor systems were studied in relation to the mechanism of action and adverse effects of ECT. In the noradrenergic system, chronically administered ECS, along with other effective antidepressant treatments, has been consistently reported to down-regulate beta-adrenergic receptors in rat cerebral cortex. Even when ECS was administered according to an intermittent clinically equivalent schedule, a 21% reduction in cortical 3H-DHA binding to beta-adrenoreceptors could be demonstrated 4 days after the last treatment. However, the role of presynaptic NA events in beta-adrenoreceptor down-regulation by ECS and the antidepressant mechanism of ECT remains to be clarified. Compared to the MAO inhibitor clorgyline, repeated ECS pretreatment induced only a moderate increase in NA release from a rat cortical vesicular preparation and minimally reduced the sensitivity of the preparation to release-inhibition by clonidine. In the dopaminergic system, a clinically equivalent ECS schedule had no direct effect on behavioral or biochemical indices of DA receptor sensitivity. However, the same ECS schedule significantly attenuated haloperidol-induced behaviorally and biochemically measured DA supersensitivity in the same model in which parallel effects had been reported for lithium. The possibility that a "receptor-stabilizing" mechanism may be common to ECT and lithium is considered on the basis of similarities in the clinical profiles of the two treatments. In the cholinergic system, repeated ECS significantly reduced 3H-QNB binding to muscarinic cholinergic receptors in rat cerebral cortex and hippocampus. Concurrently administered ECS also blocked the increase in 3H-QNB binding caused by chronic atropine administration. ECS effects on muscarinic cholinergic receptors may have relevance to the antidepressant mechanism of ECT.(ABSTRACT TRUNCATED AT 250 WORDS)
针对电休克治疗（ECT）的作用机制及不良反应，研究了电惊厥休克（ECS）在三种神经递质 - 受体系统中的神经化学效应。在去甲肾上腺素能系统中，长期给予ECS以及其他有效的抗抑郁治疗，一直有报道称会使大鼠大脑皮层中的β - 肾上腺素能受体下调。即使按照间歇性临床等效方案给予ECS，在最后一次治疗4天后，仍可证明皮层3H - DHA与β - 肾上腺素受体的结合减少了21%。然而，突触前去甲肾上腺素（NA）事件在ECS导致的β - 肾上腺素受体下调及ECT抗抑郁机制中的作用仍有待阐明。与单胺氧化酶（MAO）抑制剂氯吉兰相比，重复的ECS预处理仅使大鼠皮层囊泡制剂中的NA释放适度增加，且对制剂对可乐定释放抑制的敏感性影响极小。在多巴胺能系统中，临床等效的ECS方案对多巴胺（DA）受体敏感性的行为或生化指标无直接影响。然而，相同的ECS方案在同一模型中显著减弱了氟哌啶醇诱导的行为和生化测量的DA超敏反应，在该模型中锂也有类似的平行效应。基于两种治疗临床特征的相似性，考虑了“受体稳定”机制可能是ECT和锂所共有的可能性。在胆碱能系统中，重复的ECS显著降低了大鼠大脑皮层和海马中3H - QNB与毒蕈碱胆碱能受体的结合。同时给予的ECS也阻断了长期给予阿托品引起的3H - QNB结合增加。ECS对毒蕈碱胆碱能受体的影响可能与ECT的抗抑郁机制有关。（摘要截取自250字）
