REM sleep triggers a potent suppression of postural muscle tone - i.e., REM atonia. However, motor control during REM sleep is paradoxical because overall brain activity is maximal, but motor output is minimal. The skeletal motor system remains quiescent during REM sleep because somatic motoneurons are powerfully inactivated. Determining the mechanisms triggering loss of motoneuron function during REM sleep is important because breakdown in REM sleep motor control underlies sleep disorders such as REM sleep behavior disorder (RBD) and cataplexy/narcolepsy. For example, RBD is characterized by dramatic REM motor activation resulting in dream enactment and subsequent patient injury. In contrast, cataplexy a pathognomonic symptom of narcolepsy - is caused by the involuntary onset of REM-like atonia during wakefulness. This review highlights recent work from my laboratory that examines how motoneuron function is lost during normal REM sleep and it also identifies potential biochemical mechanisms underlying abnormal motor control in both RBD and cataplexy. First, I show that both GABAB and GABAA/glycine mediated inhibition of motoneurons is required for generating REM atonia. Next, I show that impaired GABA and glycine neurotransmission triggers the cardinal features of RBD in a transgenic mouse model. Last, I show that loss of an excitatory noradrenergic drive onto motoneurons is, at least in part, responsible for the loss of postural muscle tone during cataplexy in narcoleptic mice. Together, this research indicates that multiple transmitters systems are responsible for regulating postural muscle tone during REM sleep, RBD and cataplexy.

中文翻译：

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快速眼动睡眠，快速眼动睡眠行为障碍和瘫痪/发作性睡病期间运动神经元功能和肌肉张力的控制。

REM睡眠可有效抑制姿势肌张力-即REM失语症。但是，REM睡眠期间的运动控制是自相矛盾的，因为整体大脑活动最大，而运动输出却最小。REM睡眠期间骨骼运动系统保持静止，因为体细胞运动神经元被强烈失活。确定快速眼动睡眠期间触发运动神经元功能丧失的机制非常重要，因为快速眼动睡眠运动控制的崩溃是诸如快速眼动睡眠行为障碍（RBD）和瘫痪/发作性睡病等睡眠障碍的基础。例如，RBD的特征是剧烈的REM运动激活，导致梦境的形成和随后的患者伤害。相比之下，瘫痪是发作性睡病的病态症状-是由清醒过程中的REM样肌萎缩的非自愿发作引起的。这篇综述着重介绍了我实验室最近的一项工作，该工作研究了正常REM睡眠期间运动神经元功能如何丧失，还鉴定了RBD和脑瘫患者异常运动控制的潜在生化机制。首先，我表明，GABAB和GABAA /甘氨酸介导的对运动神经元的抑制都需要产生REM失语症。接下来，我证明在转基因小鼠模型中，受损的GABA和甘氨酸神经传递会触发RBD的基本特征。最后，我证明了兴奋性去甲肾上腺素能神经元对运动神经元的驱动丧失，至少部分原因是导致发作性麻醉小鼠在瘫痪时姿势肌张力的丧失。总之，这项研究表明，多个发射器系统负责在REM睡眠，RBD和瘫痪期间调节姿势性肌张力。