Hypoglossal motoneurons are postsynaptically inhibited during carbachol-induced rapid eye movement sleep

The obstructive sleep apnea syndrome is characterized by the occurrence of cyclic snoring and frequent apneic episodes during sleep, with consequent h ypoxia and hypercapnia.(12) Obstructive sleep apnea syndrome is associated with excess daytime sleepiness, depression, and an increased incidence of i schemic cardiopathy, cardiac arrythmias, systemic hypertension and brain in farction.(12,13,28,29) Hypoglossal motoneurons, which innervate extrinsic a nd intrinsic muscles of the tongue, play a key role in maintaining the pate ncy of the upper airway and in the pathophysiology of obstructive sleep apn ea syndrome.(14,16,23) Based on data obtained by using extracellular record ing techniques,(19) there is a consensus that hypoglossal motoneurons cease to discharge during rapid eye movement sleep,(17,24,32) because they are d isfacilitated.(19-21) Since other somatic motoneurons are known to be posts ynaptically inhibited during rapid eye movement sleep,(6,25,27,30) we sough t to determine, by the use of intracellular recording techniques during cho linergically induced rapid eye movement sleep,(2,21,22,26,34) whether posts ynaptic inhibitory mechanisms act on hypoglossal motoneurons. We found that , during this state, a powerful glycinergic premotor inhibitory system acts to suppress hypoglossal motoneurons. This finding opens new avenues for th e treatment of obstructive sleep apnea syndrome, and provides a foundation to explore the neural and pharmacological control of respiration-related mo toneurons during rapid eye movement sleep. (C) 1999 IBRO, Published by Else vier Science Ltd.