研究人员在最新出版的《自然—神经科学》（Nature Neuroscience）期刊上报告说，某种生产突触抑制的受体能调控它启动睡眠所需要的时间。新研究解剖了存在于各种不同失眠症背后的生物学机理。
果蝇被用作研究睡眠的模式动物，因为它们能重复哺乳类动物的许多睡眠特征。这种研究并没有证实可作为人类失眠症药物靶标的通道也适用于果蝇，然而，它提出的问题是果蝇可作为研究人类睡眠的模式动物吗？
利用遗传学和药理学方法，Leslie Griffith和同事发现了一种特殊抑制剂受体的生理学特性，它能以不同方式影响果蝇受体的下坠和睡眠保持。调控受体的减敏作用只能影响睡眠的启动，从而揭开了睡眠启动和保持的控制机理。
新工作证实了果蝇作为人类睡眼模式动物的有效性，并为特定失眠症提供了一种生物学解释。未来的研究还将探讨睡眠调控的其他方面，包括抑制受体是否有助于靶向失眠药物的设计，这种药物只针对睡眠而不影响其他方面。（来源：科学时报 王丹红）
生物谷推荐原文出处：
Nature Neuroscience 11, 354 - 359 (2008)
Published online: 27 January 2008 | doi:10.1038/nn2046
Modulation of GABAA receptor desensitization uncouples sleep onset and maintenance in Drosophila
Jose Agosto, James C Choi, Katherine M Parisky, Geoffrey Stilwell, Michael Rosbash & Leslie C Griffith
AbstractMany lines of evidence indicate that GABA and GABAA receptors make important contributions to human sleep regulation. Pharmacological manipulation of these receptors has differential effects on sleep onset and sleep maintenance insomnia. Here we show that sleep is regulated by GABA in Drosophila and that a mutant GABAA receptor, RdlA302S, specifically decreases sleep latency. The drug carbamazepine (CBZ) has the opposite effect on sleep; it increases sleep latency as well as decreasing sleep. Behavioral and physiological experiments indicated that RdlA302S mutant flies are resistant to the effects of CBZ on sleep latency and that mutant RDLA302S channels are resistant to the effects of CBZ on desensitization, respectively. These results suggest that this biophysical property of the channel, specifically channel desensitization, underlies the regulation of sleep latency in flies. These experiments uncouple the regulation of sleep latency from that of sleep duration and suggest that the kinetics of GABAA receptor signaling dictate sleep latency.
