Combined antagonism of aminergic excitatory and amino acid inhibitory receptors in the XII nucleus abolishes REM sleep-like depression of hypoglossal motoneuronal activity

摘要

During REM sleep, many central neurons increase their activity while somatosensory transmission and motor tone are suppressed (4, 6, 31, 35). Four distinct neurochemical mechanisms acting at the motoneuronal level have been proposed to cause the motor atonia of REM sleep. Two rely on active, state-specific inhibition mediated by glycine and/or GABA_A receptors (7, 26); two are disfacilitatory and based on a REM sleep-related withdrawal of motoneuronal excitation mediated by serotonin (5-HT) and norepinephrine (17, 22).