Cells of a common developmental origin regulate REM/non-REM sleep and wakefulness in mice
Cells of a common developmental origin regulate REM/non-REM sleep and wakefulness in mice
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DOI：
10.1126/science.aad1023
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发表时间：
2015-11-20
期刊：
影响因子：
56.9
通讯作者：
Itohara, Shigeyoshi
中科院分区：
文献类型：
--
作者：
Hayashi, Yu;Kashiwagi, Mitsuaki;Itohara, Shigeyoshi
哺乳动物睡眠包括快速眼动（REM）睡眠和非REM（NREM）睡眠。为了从脑干脑桥神经元的复杂混合物中分离出参与REM和NREM睡眠之间切换的神经元，我们对小鼠特定胚胎细胞谱系的神经元进行了化学遗传操作。我们鉴定了抑制REM睡眠和促进NREM睡眠的兴奋性多巴胺能神经元。这些神经元与促进觉醒的神经元有共同的发育起源;两者都来源于胚胎第10.5天表达Atoh 1的前神经后脑细胞库。我们还发现了抑制性γ-氨基丁酸释放神经元，它们在下游起作用，抑制REM睡眠。人为减少或延长REM睡眠反过来又影响了随后的NREM睡眠中的慢波活动，暗示REM睡眠在NREM睡眠的调节中。
Mammalian sleep comprises rapid eye movement (REM) sleep and non-REM (NREM) sleep. To functionally isolate from the complex mixture of neurons populating the brainstem pons those involved in switching between REM and NREM sleep, we chemogenetically manipulated neurons of a specific embryonic cell lineage in mice. We identified excitatory glutamatergic neurons that inhibit REM sleep and promote NREM sleep. These neurons shared a common developmental origin with neurons promoting wakefulness; both derived from a pool of proneural hindbrain cells expressing Atoh1 at embryonic day 10.5. We also identified inhibitory gamma-aminobutyric acid-releasing neurons that act downstream to inhibit REM sleep. Artificial reduction or prolongation of REM sleep in turn affected slow-wave activity during subsequent NREM sleep, implicating REM sleep in the regulation of NREM sleep.