Endogenous noradrenergic drive modulates respiratory muscle activity across sleep-wake states.
Published: 2006
Language: eng
Number of pages: 101
ISBN-13: 9780494213124
Description: Perfusion of the terazosin into the HMN decreased respiratory-related GG-activity in wakefulness and non-rapid eye movement (REM)-sleep; tonic GG-activity was also decreased in wakefulness. Application of phenylephrine increased GG-activity across all sleep-wake states. There was evidence of an additive effect of combined alpha1-adrenergic and 5-HT2-receptor stimulation at the HMN.These results show the first demonstration of an endogenous drive to respiratory motoneurons that activates GG muscle in wakefulness and non-REM, but not REM-sleep. Withdrawal of this noradrenergic input may be responsible for decreases in GG-activity in sleep.Suppression of respiratory muscle activity in sleep predisposes to sleep-related breathing disorders such as obstructive sleep apnea (OSA). Our laboratory developed a model for manipulation of the hypoglossal motor nucleus (HMN), the source of motor outflow to the genioglossus(GG) muscle, in rats across sleep-wake states. Microdialysis perfused terazosin (alpha1 receptor antagonist), phenylephrine (alpha1-agonist), or a combination of phenylephrine and alpha-methyl-serotonin (5HT2-agonist) into the HMN.
Notes: Source: Masters Abstracts International, Volume: 45-03, page: 1394.

Thesis (M.Sc.)--University of Toronto, 2006.

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