Abstract
Obstructive sleep apnoea is a common and serious breathing problem that is caused by effects of sleep on pharyngeal muscle tone in individuals with narrow upper airways. There has been increasing focus on delineating the brain mechanisms that modulate pharyngeal muscle activity in the awake and asleep states in order to understand the pathogenesis of obstructive apnoeas and to develop novel neurochemical treatments. Although initial clinical studies have met with only limited success, it is proposed that more rational and realistic approaches may be devised for neurochemical modulation of pharyngeal muscle tone as the relevant neurotransmitters and receptors that are involved in sleep-dependent modulation are identified following basic experiments.
Highlights
Obstructive sleep apnoea (OSA) is a serious breathing problem that affects approximately 4% of adults [1]
There have been several previous attempts in humans to increase upper airway muscle tone and to alleviate obstructive apnoeas by neurochemical approaches, and a resurgence of interest in these approaches has occurred as knowledge of the neural systems that affect pharyngeal motor control increases
These clinical studies have met with only limited success, in large part because the basic mechanisms that underlie suppression of upper airway muscle activity in natural sleep, and the neurotransmitters and receptor subtypes that are importantly involved, have not yet been fully determined
Summary
Obstructive sleep apnoea (OSA) is a serious breathing problem that affects approximately 4% of adults [1]. This effect may explain why improvements in sleep-disordered breathing following L-tryptophan administration were most pronounced in those individuals with events that predominantly occurred during non-REM sleep [30] In support of this scenario, when 5-HT is applied directly to the hypoglossal motor nucleus by in vivo microdialysis to produce tonic GG muscle stimulation in naturally sleeping animals, REM sleep is associated with periods of significant phasic suppression of GG muscle activity that can overcome this 5-HT mediated excitation [23]. Inhibitory neurotransmitters: γ-aminobutyric acid and glycine Postsynaptic inhibitory mechanisms play a role in hypotonia of postural (lumbar) and trigeminal motor neurones both in natural REM sleep and in the REM-like state produced by pontine carbachol [43,44] Whether such inhibitory mechanisms contribute to suppression of hypoglossal motor output to GG muscle in REM sleep is uncertain, on the basis of studies in decerebrate or anaesthetized animals following carbachol administration [45,46]. As for transmitters other than 5-HT, there is a distinct lack of data regarding the potential role of inhibitory neurotransmitters in control of pharyngeal muscles and its relevance to OSA
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