Rapid eye movement (REM) sleep disturbances are prevalent in various psychiatric disorders. However, the neural circuits that regulate REM sleep remain poorly understood. Here, we found that in male mice, optogenetic activation of rostromedial tegmental nucleus (RMTg) GABAergic neurons immediately converted REM sleep to arousal and then initiated non-REM (NREM) sleep. Conversely, laser-mediated inactivation completely converted NREM to REM sleep and prolonged REM sleep duration. The activity of RMTg GABAergic neurons increased to a high discharge level at the termination of REM sleep. RMTg GABAergic neurons directly converted REM sleep to wakefulness and NREM sleep via inhibitory projections to the laterodorsal tegmentum (LDT) and lateral hypothalamus (LH), respectively. Furthermore, LDT glutamatergic neurons were responsible for the REM sleep-wake transitions following photostimulation of the RMTg^GABA-LDT circuit. Thus, RMTg GABAergic neurons are essential for suppressing the induction and maintenance of REM sleep.

快速眼动 (REM) 睡眠障碍在各种精神疾病中很普遍。然而，人们对调节 REM 睡眠的神经回路知之甚少。在这里，我们发现在雄性小鼠中，头内侧被盖核 (RMTg) GABA 能神经元的光遗传学激活会立即将 REM 睡眠转化为觉醒，然后启动非 REM (NREM) 睡眠。相反，激光介导的失活将 NREM 睡眠完全转变为 REM 睡眠，并延长了 REM 睡眠时间。RMTg GABAergic 神经元的活动在 REM 睡眠结束时增加到高放电水平。RMTg GABAergic 神经元通过抑制性投射分别将 REM 睡眠转化为觉醒和 NREM 睡眠到外侧被盖 (LDT) 和外侧下丘脑 (LH)。此外，^GABA -LDT 电路。因此，RMTg GABA 能神经元对于抑制 REM 睡眠的诱导和维持至关重要。