Together, this research indicates that multiple transmitters systems are responsible for regulating postural muscle tone during REM sleep, RBD and cataplexy. ![]() The Kleine-Levin syndrome, a very rare disorder in adolescent boys, resembles narcolepsy. 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. Type 1: Narcolepsy due to hypocretin deficiency and accompanied by cataplexy (momentary muscular weakness or paralysis evoked by sudden emotional reactions) Type 2: Narcolepsy with normal hypocretin levels and without cataplexy. Next, I show that impaired GABA and glycine neurotransmission triggers the cardinal features of RBD in a transgenic mouse model. First, I show that both GABAB and GABAA/glycine mediated inhibition of motoneurons is required for generating REM atonia. 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. In contrast, cataplexy a pathognomonic symptom of narcolepsy - is caused by the involuntary onset of REM-like atonia during wakefulness. For example, RBD is characterized by dramatic REM motor activation resulting in dream enactment and subsequent patient injury. ![]() 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. Yet, the most prevalent causes of cataplexy without narcolepsy are rare genetic diseases which explains why cataplexy is classically linked to narcolepsy. ![]() The skeletal motor system remains quiescent during REM sleep because somatic motoneurons are powerfully inactivated. However, motor control during REM sleep is paradoxical because overall brain activity is maximal, but motor output is minimal. REM sleep triggers a potent suppression of postural muscle tone - i.e., REM atonia.
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