Interneurons control brain arousal states The underlying circuit mechanisms coordinating brain arousal and motor activity are poorly understood. Liu et al. found that glutamic acid decarboxylase 2 (GAD2)–expressing, but not parvalbumin-expressing, interneurons in a part of the brain known as the substantia nigra promote sleep (see the Perspective by Wisden and Franks). Parvalbuminergic neurons fire at higher rates in states of high motor activity, and their activation increases movement termination consistent with the function of the substantia nigra in suppressing unwanted movements during action selection. By contrast, GAD2 neurons are preferentially active in states of low motor activity. In addition to motor suppression, their activation powerfully enhances the transition from quiet wakefulness to sleep, which differ mainly in the arousal level rather than motor behavior. GAD2 interneurons thus provide general suppression of both motor activity and brain arousal to promote states of quiescence. Science, this issue p. 440; see also p. 366 Different populations of inhibitory interneurons are associated with activation and suppression of movement during wakefulness and sleep. The arousal state of the brain covaries with the motor state of the animal. How these state changes are coordinated remains unclear. We discovered that sleep–wake brain states and motor behaviors are coregulated by shared neurons in the substantia nigra pars reticulata (SNr). Analysis of mouse home-cage behavior identified four states with different levels of brain arousal and motor activity: locomotion, nonlocomotor movement, quiet wakefulness, and sleep; transitions occurred not randomly but primarily between neighboring states. The glutamic acid decarboxylase 2 but not the parvalbumin subset of SNr γ-aminobutyric acid (GABA)–releasing (GABAergic) neurons was preferentially active in states of low motor activity and arousal. Their activation or inactivation biased the direction of natural behavioral transitions and promoted or suppressed sleep, respectively. These GABAergic neurons integrate wide-ranging inputs and innervate multiple arousal-promoting and motor-control circuits through extensive collateral projections.

中文翻译：

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黑质中睡眠和运动控制的共同枢纽

中间神经元控制大脑唤醒状态 协调大脑唤醒和运动活动的潜在电路机制知之甚少。刘等人。发现在称为黑质的大脑部分中表达谷氨酸脱羧酶 2 (GAD2) 但不表达小清蛋白的中间神经元促进睡眠（参见 Wisden 和 Franks 的观点）。Parvalbuminergic 神经元在高运动活动状态下以更高的速率激发，并且它们的激活增加了运动终止，这与黑质在动作选择期间抑制不需要的运动的功能一致。相比之下，GAD2 神经元在低运动活动状态下优先活跃。除了运动抑制之外，它们的激活有力地增强了从安静清醒到睡眠的过渡，主要区别在于唤醒水平而不是运动行为。因此，GAD2 中间神经元提供对运动活动和大脑唤醒的普遍抑制，以促进静止状态。科学，这个问题 p。440; 另见第 366 不同群体的抑制性中间神经元与清醒和睡眠期间运动的激活和抑制有关。大脑的唤醒状态随动物的运动状态而变化。如何协调这些状态变化仍不清楚。我们发现睡眠-觉醒的大脑状态和运动行为是由黑质网状部 (SNr) 中的共享神经元共同调节的。对小鼠家笼行为的分析确定了具有不同程度的大脑唤醒和运动活动的四种状态：运动、非运动运动、安静清醒和睡眠；转换不是随机发生的，而是主要发生在相邻状态之间。谷氨酸脱羧酶 2 但不是 SNr γ-氨基丁酸 (GABA) 释放（GABA 能）神经元的小清蛋白子集，在低运动活动和唤醒状态下优先活跃。它们的激活或失活分别偏向了自然行为转变的方向，并分别促进或抑制了睡眠。这些 GABA 能神经元整合了广泛的输入，并通过广泛的侧枝投射来支配多个促进唤醒和运动控制的回路。它们的激活或失活分别偏向了自然行为转变的方向，并分别促进或抑制了睡眠。这些 GABA 能神经元整合了广泛的输入，并通过广泛的侧枝投射来支配多个促进唤醒和运动控制的回路。它们的激活或失活分别偏向了自然行为转变的方向，并分别促进或抑制了睡眠。这些 GABA 能神经元整合了广泛的输入，并通过广泛的侧枝投射来支配多个促进唤醒和运动控制的回路。