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Published ahead of print on August 11, 2005, doi:10.1164/rccm.200412-1750OC

Am. J. Respir. Crit. Care Med., Volume 172, Number 10, November 2005, 1322-1330

A more recent version of this article appeared on November 15, 2005
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Submitted on December 28, 2004
Accepted on August 10, 2005

REM Sleep-like Atonia of XII Motoneurons is Caused by Loss of Noradrenergic and Serotonergic Inputs

Victor B Fenik1, Richard O Davies1, and Leszek Kubin1*

1 Department of Animal Biology, University of Pennsylvania, School of Veterinary Medicine, Philadelphia, PA, USA; Center for Sleep and Respiratory Neurobiology, University of Pennsylvania, Philadelphia, PA, USA

* To whom correspondence should be addressed. E-mail: lkubin{at}vet.upenn.edu.

Rationale: 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. Objectives: 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 prior to, and at different times after, combined microinjections of prazosin and methysergide, or only one of the drugs, into the XII nucleus. Measurements and Main Results: Spontaneous XII nerve activity was significantly reduced, by 35-81%, by each antagonist alone and in combination, indicating that XII motoneurons were under both noradrenergic and serotonergic endogenous excitatory drives. During the period 32-81 min following microinjections of both antagonists, pontine carbachol caused no depression of XII nerve activity, whereas other characteristic effects (activation of the hippocampal and cortical EEG, 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.
Key words: hypoglossal motoneurons, norepinephrine, obstructive sleep apnea, serotonin, pons




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