研究人員在最新出版的《自然—神經(jīng)科學(xué)》（Nature Neuroscience）期刊上報(bào)告說，某種生產(chǎn)突觸抑制的受體能調(diào)控它啟動(dòng)睡眠所需要的時(shí)間,。新研究解剖了存在于各種不同失眠癥背后的生物學(xué)機(jī)理,。
果蠅被用作研究睡眠的模式動(dòng)物,，因?yàn)樗鼈兡苤貜?fù)哺乳類動(dòng)物的許多睡眠特征,。這種研究并沒有證實(shí)可作為人類失眠癥藥物靶標(biāo)的通道也適用于果蠅，然而,，它提出的問題是果蠅可作為研究人類睡眠的模式動(dòng)物嗎,？
利用遺傳學(xué)和藥理學(xué)方法，Leslie Griffith和同事發(fā)現(xiàn)了一種特殊抑制劑受體的生理學(xué)特性,，它能以不同方式影響果蠅受體的下墜和睡眠保持,。調(diào)控受體的減敏作用只能影響睡眠的啟動(dòng)，從而揭開了睡眠啟動(dòng)和保持的控制機(jī)理,。
新工作證實(shí)了果蠅作為人類睡眼模式動(dòng)物的有效性,，并為特定失眠癥提供了一種生物學(xué)解釋。未來的研究還將探討睡眠調(diào)控的其他方面,，包括抑制受體是否有助于靶向失眠藥物的設(shè)計(jì),，這種藥物只針對(duì)睡眠而不影響其他方面。（來源：科學(xué)時(shí)報(bào) 王丹紅）
生物谷推薦原文出處：
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.
