Abstract
Obstructive Sleep Apnea (OSA) is a common sleep-related respiratory disorder that is associated with cognitive, cardiovascular, and metabolic morbidities. The major cause of OSA is the sleep-related reduction of upper airway muscle tone that leads to airway obstructions in individuals with anatomically narrow upper airway. This reduction is mainly due to the suppressant effect of sleep on hypoglossal motoneurons that innervate upper airway muscles. The hypoglossal motoneurons have state-dependent activity, which is decreased during the transition from wakefulness to non-rapid eye movement sleep and is further suppressed during rapid eye movement sleep. Multiple neurotransmitters and their receptors have been implicated in the control of hypoglossal motoneuron activity across the sleep-wake states. However, to date, the results of the rigorous testing show that withdrawal of noradrenergic excitation and cholinergic inhibition essentially contribute to the depression of hypoglossal motoneuron activity during sleep. The present review will focus on origins of noradrenergic and cholinergic innervation of hypoglossal motoneurons and the functional role of these neurons in the state-dependent activity of hypoglossal motoneurons.
Highlights
NEUROTRANSMITTERS IMPLICATED IN THE CONTROL OF HYPOGLOSSAL MOTONEURONSObstructive Sleep Apnea (OSA) is a sleep-related breathing disorder characterized by repetitive nocturnal apnea/hypopnea episodes due to partial or complete closure of upper airway [1,2,3,4,5]
Reviewed by: Satvinder Kaur, Beth Israel Deaconess Medical Center, Harvard Medical School, United States Viliam Donic, University of Pavol Jozef Šafárik, Slovakia
The glycinergic nature of the inhibition of hypoglossal motoneuron activity during rapid eye movement (REM) sleep was hypothesized based on the findings that strychnine, a glycine receptor antagonist, abolished large postsynaptic hyperpolarizing potentials that appeared in REM sleep during intracellular recording of hypoglossal motoneurons [28]
Summary
Obstructive Sleep Apnea (OSA) is a sleep-related breathing disorder characterized by repetitive nocturnal apnea/hypopnea episodes due to partial or complete closure of upper airway [1,2,3,4,5]. In most OSA patients, the nocturnal apneic episodes result from anatomical abnormalities of upper airway aperture that are combined with the sleep-related depression of upper airway muscle tone [3, 5]. The elevated activity of upper airway muscles, including the genioglossus muscle, keeps the airway open during wakefulness in OSA patients [18]. Their activity is reduced during non-rapid eye movement (NREM) sleep and further suppressed during rapid eye movement (REM) sleep [2, 13, 16, 18,19,20,21,22,23]. Multiple neurotransmitters have been implicated in the control of state-dependent activity of hypoglossal motoneurons [reviewed by [24,25,26,27]]
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