Abstract
Hypocretin deficiency is involved in most cases of human narcolepsy. Although cataplexy is pathognomonic of narcolepsy, mechanisms of induction of cataplexy are largely unknown. Patterns of occurrence of cataplectic attacks (i.e. onset location, laterality, and propagation of attacks) in hypocretin receptor 2-mutated narcoleptic Dobermans were characterized in order to understand the basic mechanism of this abnormal sleep-related atonia. Most cataplexy attacks were bilateral (98%) and were initiated in the hind legs (80%). Progression of attacks was also seen (49%) and atonia during propagation was most often bilateral (94%). Involvement of abnormal inactivation of bilateral pathways to the spinal motoneurones due to a deficiency in hypocretin neurotransmission is suggested in the occurrence of cataplexy.
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