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GABA 能受体脱敏作为佐匹克隆诱导梦游的机制。

Desensitization of GABAergic receptors as a mechanism of zolpidem-induced somnambulism.

机构信息

Department of Animal Behavior, Institute of Genetics and Animal Breeding, Jastrzebiec, Poland.

出版信息

Med Hypotheses. 2011 Aug;77(2):230-3. doi: 10.1016/j.mehy.2011.04.019. Epub 2011 May 11.

DOI:10.1016/j.mehy.2011.04.019
PMID:21565448
Abstract

Sleepwalking is a frequently reported side effect of zolpidem which is a short-acting hypnotic drug potentiating activity of GABA(A) receptors. Paradoxically, the most commonly used medications for somnambulism are benzodiazepines, especially clonazepam, which also potentiate activity of GABA(A) receptors. It is proposed that zolpidem-induced sleepwalking can be explained by the desensitization of GABAergic receptors located on serotonergic neurons. According to the proposed model, the delay between desensitization of GABA receptors and a compensatory decrease in serotonin release constitutes the time window for parasomnias. The occurrence of sleepwalking depends on individual differences in receptor desensitization, autoregulation of serotonin release and drug pharmacokinetics. The proposed mechanism of interaction between GABAergic and serotonergic systems can be also relevant for zolpidem abuse and zolpidem-induced hallucinations. It is therefore suggested that special care should be taken when zolpidem is used in patients taking at the same time selective serotonin reuptake inhibitors.

摘要

梦游是佐匹克隆的常见副作用之一,佐匹克隆是一种作用时间短的催眠药物,可增强 GABA(A)受体的活性。矛盾的是,最常用于治疗梦游症的药物是苯二氮䓬类药物,尤其是氯硝西泮,它也可增强 GABA(A)受体的活性。据推测,佐匹克隆引起的梦游可以用位于 5-羟色胺能神经元上的 GABA 能受体脱敏来解释。根据提出的模型,GABA 受体脱敏和 5-羟色胺释放代偿性减少之间的延迟构成了发生睡眠障碍的时间窗口。梦游的发生取决于受体脱敏、5-羟色胺释放的自身调节和药物药代动力学的个体差异。GABA 能和 5-羟色胺能系统之间相互作用的提出机制也可能与佐匹克隆滥用和佐匹克隆引起的幻觉有关。因此,建议在同时服用选择性 5-羟色胺再摄取抑制剂的患者中使用佐匹克隆时应特别小心。

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