快眼动（REM）睡眠障碍已成为严重的医学问题，由于机制不明，临床缺乏对策。揭示REM睡眠障碍的机制成为睡眠研究领域重要的科学问题。损毁脑桥外侧被盖核(LPT)，REM睡眠明显增加；REM睡眠剥夺使LPT神经元活性增加。我们预实验光遗传学激活LPT中GABA能神经元，REM睡眠立即停止。我们假说：LPT的GABA能神经元是REM终止神经元，通过下游的REM睡眠调控的相关核团，抑制REM睡眠。本课题拟利用GAD2-Cre小鼠、光遗传学和药理遗传学技术操控神经元活性，特异性神经纤维追踪等方法，结合睡眠解析平台、电生理、免疫组化等技术，研究LPT中GABA能神经元对REM睡眠的调控作用、神经环路和神经递质机制。预期结果将丰富和发展REM睡眠调节理论，为探索治疗REM睡眠障碍的新方法提供理论依据。

Rapid eye movement (REM) sleep disorder has become a serious medical problem. There are no effective ways to treat this sleep disorder clinically because the mechanisms are not clear. Therefore, to reveal the mechanism of REM sleep disorder has become an important scientific problem in the field of sleep research. Lesion of the lateral pontine tegmentum (LPT) significantly increased REM sleep, and REM sleep deprivation increased the activity of LPT neurons. Our preliminary data show that activation of GABAergic neuron in LPT abolished REM sleep. We therefore hypothesized that LPT GABAergic neurons are REM terminating neurons, which inhibits REM sleep through downstream REM sleep-regulated nuclei. In the present study, we are going to use GAD2-Cre mice, optogenetics and pharmacogenetic DREADD to specifically manipulate neuron activity, and the specific neuronal tract tracing, combined with cell electrophysiological, immunohistochemistry, and automatic sleep bioassay systems to study the role of LPT GABAergic neuron in regulation of REM sleep behaviors, and the neural circuits and neurotransmitter involved. The expected findings will enrich and develop the theory of REM sleep regulation, and provide theoretical basis for the treatment of REM sleep disorders.