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脑内去甲肾上腺素耗竭可阻止电休克惊厥诱导的5-羟色胺和多巴胺介导行为的增强。

Brain noradrenaline depletion prevents ECS-induced enhancement of serotonin- and dopamine-mediated behaviour.

作者信息

Green A R, Deakin J F

出版信息

Nature. 1980 May 22;285(5762):232-3. doi: 10.1038/285232a0.

Abstract

When rats are given a series of electroconvulsive shocks (ECSs) over several days, they display enhanced behavioural responses to both serotonin- and dopamine-receptor agonists. Because these changes are seen when the ECS is given in ways closely mimicking the clinical administration of electroconvulsive therapy (ECT), it has been suggested that the changes in postsynaptic monoamine function may be involved in the antidepressant mechanisms of ECT. Ligand-binding studies have excluded the possibility that ECS alters the characteristics of either the serotonin or dopamine receptor; ECS may therefore be acting on neuronal systems which modulate monoamine neurotransmission. As repeated ECS has recently been reported to decrease both noradrenaline (NA)-sensitive adenylate cyclase and beta-adrenoreceptor binding, we have examined here whether changes in NA function are related to the effects of ECS on the serotonin- and dopamine-mediated behaviours. We demonstrate that although selective depletion of NA does not alter the drug-induced serotonin- and dopamine-mediated responses, it abolishes the ECS-induced enhancement of these behaviours.

摘要

当大鼠在数天内接受一系列电惊厥休克(ECS)时,它们对血清素和多巴胺受体激动剂均表现出增强的行为反应。由于当以紧密模拟电惊厥治疗(ECT)临床给药方式给予ECS时会出现这些变化,因此有人提出突触后单胺功能的变化可能参与了ECT的抗抑郁机制。配体结合研究排除了ECS改变血清素或多巴胺受体特性的可能性;因此,ECS可能作用于调节单胺神经传递的神经元系统。由于最近报道重复ECS会降低去甲肾上腺素(NA)敏感的腺苷酸环化酶和β-肾上腺素能受体结合,我们在此研究了NA功能的变化是否与ECS对血清素和多巴胺介导行为的影响有关。我们证明,虽然选择性耗尽NA不会改变药物诱导的血清素和多巴胺介导的反应,但它会消除ECS诱导的这些行为增强。

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