The Roles of Hypocretin/Orexin in Narcolepsy, Parkinson’s Disease, and Normal Behavior

Abstract

Animal studies have shown that cataplexy is correlated with a characteristic pattern of neuronal activity. There is strong activation of a restricted population of medial medullary neurons presumed to release GABA and glycine onto motoneurons. At the same time, most glutamatergic medial reticular neurons, which are active during REM sleep and waking movement, fall silent. Noradrenergic neurons which provide a tonic depolarizing input to motoneurons fall silent in tight temporal correlation with the loss of muscle tone. However, histamine neurons, which are silent in REM sleep, remain active during cataplexy. Most human narcolepsy with cataplexy is caused by a loss of hcrt cells and at least one case of narcolepsy without cataplexy has been characterized by a loss of posterior hypothalamic hcrt cells. Narcolepsy-like symptoms in Parkinson's disease may also be caused by hcrt cell loss. In intact animals, hcrt cell activity has little relation to feeding, but does appear to be correlated with arousal linked to positive emotions. (PsycINFO Database Record (c) 2020 APA, all rights reserved)