Abstract：
Rapid eye movement (REM) sleep has been hypothesized to promote emotional resilience, but any neuronal circuits mediating this have not been identified. We find that in mice, somatostatin (Som) neurons in the entopeduncular nucleus (EPSom)/internal globus pallidus are predominantly active during REM sleep. This unique REM activity is both necessary and sufficient for maintaining normal REM sleep. Inhibiting or exciting EPSom neurons reduced or increased REM sleep duration, respectively. Activation of the sole downstream target of EPSom neurons, Vglut2 cells in the lateral habenula (LHb), increased sleep via the ventral tegmental area (VTA). A simple chemogenetic scheme to periodically inhibit the LHb over 4 days selectively removed a significant amount of cumulative REM sleep. Chronic, but not acute, REM reduction correlated with mice becoming anxious and more sensitive to aversive stimuli. Therefore, we suggest that cumulative REM sleep, in part generated by the EP → LHb → VTA circuit identified here, could contribute to stabilizing reactions to habitual aversive stimuli.
摘要：
快速眼动（REM）睡眠被认为可以促进情绪弹性，但是尚未发现任何介导这种情况的神经元回路。我们发现在老鼠身上，在REM睡眠期间，足盘核（EPSom）/内部苍白球中的生长抑素（Som）神经元主要活跃。这种独特的REM活动对于维持正常的REM睡眠是必要和充分的。抑制或刺激EPSom神经元减少或增加REM睡眠持续时间，分别。激活EPSom神经元的唯一下游靶标，Vglut2细胞在侧突（LHb），通过腹侧被盖区（VTA）增加睡眠。在4天内定期抑制LHb的简单化学遗传方案选择性地去除大量的累积REM睡眠。慢性,但不是急性的，REM减少与小鼠变得焦虑和对厌恶刺激更敏感相关。因此,我们建议累积快速眼动睡眠，部分由此处标识的EP→LHb→VTA电路生成，可能有助于稳定对习惯性厌恶刺激的反应。
