title: REM sleep-like atonia of hypoglossal (XII) motoneurons is caused by loss of noradrenergic and serotonergic inputs.
abstract: BACKGROUND
  Studies of hypoglossal (XII) motoneurons that innervate the genioglossus muscle, an upper airway dilator, suggested that the suppression of upper airway motor tone during REM sleep is caused by withdrawal of excitation mediated by norepinephrine and serotonin.
  
  
  OBJECTIVE
  Our objectives were to determine whether antagonism of aminergic receptors located in the XII nucleus region can abolish the REM sleep-like atonia of XII motoneurons, and whether both serotonergic and noradrenergic antagonists are required to achieve this effect.
  
  
  METHODS
  REM sleep-like episodes were elicited in anesthetized rats by pontine carbachol injections before and at various times after microinjection of prazosin and methysergide combined, or of only one of the drugs, into the XII nucleus.
  
  
  RESULTS
  Spontaneous XII nerve activity was significantly reduced, by 35 to 81%, by each antagonist alone and in combination, indicating that XII motoneurons were under both noradrenergic and serotonergic endogenous excitatory drives. During the 32 to 81 min after microinjections of both antagonists, pontine carbachol caused no depression of XII nerve activity, whereas other characteristic effects (activation of the hippocampal and cortical EEG, and slowing of the respiratory rate) remained intact. A partial recovery of the depressant effect of carbachol then occurred parallel to the recovery of spontaneous XII nerve activity from the depressant effect of the antagonists. Microinjections of either antagonist alone did not eliminate the depressant effect of carbachol.
  
  
  CONCLUSIONS
  The REM sleep-like depression of XII motoneuronal activity induced by pontine carbachol can be fully accounted for by the combined withdrawal of noradrenergic and serotonergic effects on XII motoneurons.
authors.affiliation: Department of Animal Biology, 209E/VET, School of Veterinary Medicine, University of Pennsylvania, 3800 Spruce Street, Philadelphia, Pennsylvania 19104-6046, USA.
authors.forename: Victor B
authors.initials: VB
authors.lastname: Fenik
authors.forename: Richard O
authors.initials: RO
authors.lastname: Davies
authors.forename: Leszek
authors.initials: L
authors.lastname: Kubin
mesh_terms: D018674:Adrenergic Antagonists / Q000494:pharmacology; D000818:Animals; D018680:Cholinergic Antagonists / Q000494:pharmacology; D007002:Hypoglossal Nerve / Q000166:cytology / Q000502:physiology*; D008784:Methysergide / Q000494:pharmacology; D009046:Motor Neurons / Q000473:pathology / Q000502:physiology*; D009638:Norepinephrine / Q000378:metabolism; D011224:Prazosin / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017981:Receptors, Neurotransmitter / Q000187:drug effects / Q000378:metabolism*; D012132:Respiratory Muscles / Q000294:innervation*; D012701:Serotonin / Q000378:metabolism; D012895:Sleep, REM / Q000502:physiology*
chemical_list: D018674:Adrenergic Antagonists; D018680:Cholinergic Antagonists; D017981:Receptors, Neurotransmitter; D012701:Serotonin; D009638:Norepinephrine; D011224:Prazosin; D008784:Methysergide