REM Sleep at its Core - Circuits, Neurotransmitters, and Pathophysiology.
REM Sleep at its Core - Circuits, Neurotransmitters, and Pathophysiology.
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DOI：
10.3389/fneur.2015.00123
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发表时间：
2015
影响因子：
3.4
通讯作者：
Peever JH
中科院分区：
文献类型：
--
作者：
Fraigne JJ;Torontali ZA;Snow MB;Peever JH
快速眼动（REM）睡眠是由脑干、前脑和下丘脑的多种神经递质系统相互作用产生和维持的。在这些回路中有一个核心区域，在快速眼动睡眠期间活跃，被称为蓝下核（SubC）或气味下核。据推测，谷氨酸能亚c神经元调节快速眼动睡眠及其定义特征，如肌肉麻痹和皮层激活。当谷氨酸能亚c细胞激活内侧髓质腹侧的神经元，导致GABA和甘氨酸释放到骨骼运动神经元时，REM睡眠麻痹就开始了。REM睡眠时间受脑干腹外侧导水管周围灰核和背侧副巨细胞网状核的gaba能神经元、下丘脑的黑色素浓缩激素神经元和脑干背侧和桥脚被的胆碱能细胞的活动控制。确定这些回路如何与亚皮层相互作用是很重要的，因为它们之间的交流中断被认为是发作性睡病/猝厥和快速眼动睡眠行为障碍（RBD）的基础。这篇综述综合了我们目前对产生健康快速眼动睡眠的机制的理解，以及这些回路的功能障碍如何导致常见的快速眼动睡眠障碍，如猝厥/发作性睡病和RBD。
Rapid eye movement (REM) sleep is generated and maintained by the interaction of a variety of neurotransmitter systems in the brainstem, forebrain, and hypothalamus. Within these circuits lies a core region that is active during REM sleep, known as the subcoeruleus nucleus (SubC) or sublaterodorsal nucleus. It is hypothesized that glutamatergic SubC neurons regulate REM sleep and its defining features such as muscle paralysis and cortical activation. REM sleep paralysis is initiated when glutamatergic SubC cells activate neurons in the ventral medial medulla, which causes release of GABA and glycine onto skeletal motoneurons. REM sleep timing is controlled by activity of GABAergic neurons in the ventrolateral periaqueductal gray and dorsal paragigantocellular reticular nucleus as well as melanin-concentrating hormone neurons in the hypothalamus and cholinergic cells in the laterodorsal and pedunculo-pontine tegmentum in the brainstem. Determining how these circuits interact with the SubC is important because breakdown in their communication is hypothesized to underlie narcolepsy/cataplexy and REM sleep behavior disorder (RBD). This review synthesizes our current understanding of mechanisms generating healthy REM sleep and how dysfunction of these circuits contributes to common REM sleep disorders such as cataplexy/narcolepsy and RBD.
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