最新一期美國《神經(jīng)科學(xué)雜志》發(fā)表復(fù)旦大學(xué)醫(yī)學(xué)神經(jīng)生物學(xué)國家重點(diǎn)實(shí)驗(yàn)室黃志力課題組一項(xiàng)研究成果，這一成果有望有效治療因換床導(dǎo)致無法入睡的失眠癥,。
醫(yī)學(xué)上把這種失眠現(xiàn)象稱為“第一晚效應(yīng)”,。資料顯示，隨著工業(yè)化進(jìn)程的加快,，社會(huì)競(jìng)爭(zhēng),、工作壓力，不良夜生活習(xí)慣及人口老齡化等原因,，全球三分之一的人存在睡眠問題,，其中不少人因經(jīng)常出差不能在習(xí)慣的床上睡眠或入睡前情緒改變，精神亢奮或緊張,，難以入眠,，深陷“第一晚效應(yīng)”痛苦之中,，不能自拔,，嚴(yán)重影響次日工作效率和身體健康。
研究表明,，多巴胺系統(tǒng)調(diào)控運(yùn)動(dòng),、情感、獎(jiǎng)賞,、認(rèn)知等生理過程與藥物成癮關(guān)系密切,。但人們對(duì)”多巴胺“在睡眠覺醒中的作用及機(jī)制認(rèn)識(shí)非常有限,。復(fù)旦大學(xué)醫(yī)學(xué)神經(jīng)生物學(xué)國家重點(diǎn)實(shí)驗(yàn)室黃志力課題組研究人員曲衛(wèi)敏、徐昕紅等,，運(yùn)用高度自動(dòng)化睡眠覺醒解析系統(tǒng),，記錄一種已經(jīng)基因剔除了“多巴胺D2受體”小鼠的睡眠過程，并結(jié)合藥理學(xué)等手段,，從基因到行為解析了多巴胺D2受體在睡眠覺醒調(diào)控中的作用,。
結(jié)果發(fā)現(xiàn)：與正常小鼠（野生型小鼠）相比，剔除了“多巴胺D2受體”的小鼠,，活動(dòng)期維持覺醒困難,，睡眠量增加。為模擬人在新環(huán)境下（如出差住宿等）出現(xiàn)“換床后”失眠現(xiàn)象,，即“第一晚效應(yīng)”,，研究人員更換動(dòng)物居住環(huán)境，考察小鼠在新環(huán)境中的睡眠行為,。結(jié)果顯示：多巴胺D2受體正常的小鼠面對(duì)新環(huán)境刺激,，極為不習(xí)慣，入睡困難,，而剔除了“多巴胺D2受體”的小鼠,，則“高枕無憂”，迅速入睡,。
該研究成果揭示大腦內(nèi)蛋白質(zhì)多巴胺D2受體是調(diào)控覺醒行為的重要受體,，豐富和發(fā)展了醫(yī)學(xué)界有關(guān)睡眠、覺醒調(diào)節(jié)理論系統(tǒng),，為臨床治療人群中普遍存在的“換床入睡難”的“第一晚效應(yīng)”頑癥,，提供了新思路和新方法。(生物谷Bioon.com)
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生物谷推薦原文出處：
The Journal of Neuroscience doi:10.1523/JNEUROSCI.4936-09.2010
Essential Role of Dopamine D2 Receptor in the Maintenance of Wakefulness, But Not in Homeostatic Regulation of Sleep, in Mice
Wei-Min Qu,1 Xin-Hong Xu,1 Ming-Ming Yan,1 Yi-Qun Wang,1 Yoshihiro Urade,2 and Zhi-Li Huang1
1Department of Pharmacology, State Key Laboratory of Medical Neurobiology, Shanghai Medical College of Fudan University, Shanghai 200032, China, and 2Department of Molecular Behavioral Biology, Osaka Bioscience Institute, Suita, Osaka 565-0874, Japan
Dopamine (DA) and its D2 receptor (R) are involved in cognition, reward processing, and drug addiction. However, their roles in sleep–wake regulation remain unclear. Herein we investigated the role of D2R in sleep–wake regulation by using D2R knock-out (KO) mice and pharmacological manipulation. Compared with WT mice, D2R KO mice exhibited a significant decrease in wakefulness, with a concomitant increase in non-rapid eye movement (non-REM, NREM) and REM sleep and a drastic decrease in the low-frequency (0.75–2 Hz) electroencephalogram delta power of NREM sleep, especially during the first 4 h after lights off. The KO mice had decreased mean episode duration and increased episode numbers of wake and NREM sleep, many stage transitions between wakefulness and NREM sleep during the dark period, suggesting the instability of the wake stage in these D2R KO mice. When the KO mice were subjected to a cage change or an intraperitoneal saline injection, the latency to sleep in the KO mice decreased to half of the level for WT mice. The D2R antagonist raclopride mimicked these effects in WT mice. When GBR12909, a dopamine transport inhibitor, was administered intraperitoneally, it induced wakefulness in WT mice in a dose-dependent manner, but its arousal effect was attenuated to one-third in the D2R KO mice. However, these 2 genotypes showed an identical response in terms of sleep rebound after 2, 4, and 6 h of sleep deprivation. These results indicate that D2R plays an essential role in the maintenance of wakefulness, but not in homeostatic regulation of NREM sleep.
