The neurobiology and neurophysiology of paradoxical (REM) sleep
Résumé
Rapid eye movement (REM) sleep (or paradoxical sleep [PS]) is a state character-ized by REMs, electroencephalography (EEG) activation and muscle atonia. In this review, we present the latest update on the neuronal network responsible for PS. We propose that muscle atonia during PS is due to activation of PS-on glutamatergic neurons localized in the caudal pontine sublaterodorsal tegmental nucleus (SLD) and the glycinergic/GABAergic pre-motoneurons localized in the ventro-medial medulla (vmM). The SLD neurons are inactivated during waking and slow-wave sleep by PS- off GABAergic neurons localized in the ventrolateral periaqueductal gray and the adjacent deep mesencephalic reticular nucleus. PS onset and maintenance is due to the inhibition of these PS-off neurons by PS-on GABAergic neurons localized in the posterior hypothalamus, the ventrolateral periaqueductal gray and the lateral and dorsal paragigantocellular reticular nuclei. Finally, we show that only a few limbic cortical structures are activated during PS by the claustrum and the supramammillary nucleus and discuss the possible function of such activation.
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