Abstract
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.
Highlights
Rapid eye movement (REM) sleep is characterized by rapid eye movements, cortical activation, vivid dreaming, skeletal muscle paralysis, and muscle twitches [1,2,3]
Those with REM sleep behavior disorder (RBD) suffer from the loss of normal muscle paralysis during REM sleep, which results in pathological levels of movement during REM sleep episodes
Understanding the neural circuits that generate REM sleep and REM sleep paralysis is needed in order to REM sleep mechanisms in health and disease clarify the pathophysiology of narcolepsy/cataplexy and RBD [4, 5]
Summary
Rapid eye movement (REM) sleep is characterized by rapid eye movements, cortical activation, vivid dreaming, skeletal muscle paralysis (atonia), and muscle twitches [1,2,3]. Disturbances in the normal control of REM sleep underlie cataplexy/narcolepsy and RBD, which are two common and serious sleep disorders. Cataplexy is hypothesized to result from intrusion of REM sleep paralysis into wakefulness [4]. REM sleep mechanisms in health and disease clarify the pathophysiology of narcolepsy/cataplexy and RBD [4, 5]. We discuss how REM sleep-control mechanisms underlie the intrusion of REM sleep paralysis during wakefulness in narcolepsy with cataplexy, and how degeneration of this same circuitry could underlie RBD. We discuss how newly identified hypothalamic circuits control REM sleep and how they potentially contribute to the pathophysiology of narcolepsy with cataplexy
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