title: Postsynaptic inhibition of hypoglossal motoneurons produces atonia of the genioglossal muscle during rapid eye movement sleep.
abstract: OBJECTIVE
  Hypoglossal motoneurons were recorded intracellularly to determine whether postsynaptic inhibition or disfacilitation was responsible for atonia of the lingual muscles during rapid eye movement (REM) sleep.
  
  
  METHODS
  Intracellular records were obtained of the action potentials and subthreshold membrane potential activity of antidromically identified hypoglossal motoneurons in cats during wakefulness, nonrapid eye movement (NREM) sleep, and REM sleep. A cuff electrode was placed around the hypoglossal nerve to antidromically activate hypoglossal motoneurons. The state-dependent changes in membrane potential, spontaneous discharge, postsynaptic potentials, and rheobase of hypoglossal motoneurons were determined.
  During quiet wakefulness and NREM sleep, hypoglossal motoneurons exhibited spontaneous repetitive discharge. In the transition from NREM sleep to REM sleep, repetitive discharge ceased and the membrane potential began to hyperpolarize; maximal hyperpolarization (10.5 mV) persisted throughout REM sleep. During REM sleep there was a significant increase in rheobase, which was accompanied by barrages of large-amplitude inhibitory postsynaptic potentials (IPSPs), which were reversed following the intracellular injection of chloride ions. The latter result indicates that they were mediated by glycine; IPSPs were not present during wakefulness or NREM sleep.
  
  
  CONCLUSIONS
  We conclude that hypoglossal motoneurons are postsynaptically inhibited during naturally occurring REM sleep; no evidence of disfacilitation was observed. The data also indicate that glycine receptor-mediated postsynaptic inhibition of hypoglossal motoneurons is crucial in promoting atonia of the lingual muscles during REM sleep.
authors.affiliation: VA Greater Los Angeles Healthcare System, Los Angeles, CA: Websciences International, Los Angeles, CA.
authors.forename: Simon J
authors.initials: SJ
authors.lastname: Fung
authors.affiliation: VA Greater Los Angeles Healthcare System, Los Angeles, CA: Websciences International, Los Angeles, CA: Department of Physiology, UCLA School of Medicine, Los Angeles, CA.
authors.forename: Michael H
authors.initials: MH
authors.lastname: Chase
mesh_terms: D000818:Animals; D002415:Cats; D002712:Chlorides / Q000494:pharmacology; D004558:Electric Stimulation; D007002:Hypoglossal Nerve / Q000166:cytology* / Q000502:physiology; D053444:Inhibitory Postsynaptic Potentials / Q000502:physiology*; D008297:Male; D008564:Membrane Potentials; D009046:Motor Neurons / Q000502:physiology*; D009123:Muscle Hypotonia; D009132:Muscles / Q000294:innervation / Q000502:physiology; D018009:Receptors, Glycine / Q000378:metabolism; D012895:Sleep, REM / Q000502:physiology*; D014059:Tongue / Q000294:innervation* / Q000502:physiology*; D014851:Wakefulness / Q000502:physiology
chemical_list: D002712:Chlorides; D018009:Receptors, Glycine
keywords: IPSP; OSA; REM sleep; atonia; hypoglossal; motoneuron; postsynaptic inhibition