Behavioral response and transmitter release during atonia elicited by medial medullary stimulation.

Activation of the medial medulla is responsible for rapid eye movement (REM) sleep atonia and cataplexy. Dysfunction can cause REM sleep behavior disorder and other motor pathologies. Here we report the behavioral effects of stimulation of the nucleus gigantocellularis (NGC) and nucleus magnocellularis (NMC) in unrestrained cats. In waking, 62% of the medial medullary stimulation sites suppressed muscle tone. In contrast, stimulation at all sites, including sites where stimulation produced no change or increased muscle tone in waking, produced decreased muscle tone during slow-wave sleep. In the decerebrate cat electrical stimulation of the NGC increased glycine and decreased norepinephrine (NE) release in the lumbar ventral horn, with no change in γ-aminobutyric acid (GABA) or serotonin (5-HT) release. Stimulation of the NMC increased both glycine and GABA release and also decreased both NE and 5-HT release in the ventral horn. Glutamate levels in the ventral horn were not changed by either NGC or NMC stimulation. We conclude that NGC and NMC play neurochemically distinct but synergistic roles in the modulation of motor activity across the sleep-wake cycle via a combination of increased release of glycine and GABA and decreased release of 5-HT and NE. Stimulation of the medial medulla that elicited muscle tone suppression also triggered rapid eye movements, but never produced the phasic twitches that characterize REM sleep, indicating that the twitching and rapid eye movement generators of REM sleep have separate brain stem substrates.