Abstract
The sleep-related depression of excitability of upper airway motoneurons is a major neurological cause of obstructive sleep apnea whereas a disruption in the inhibition of spinal motoneurons during rapid eye movement (REM) sleep causes the REM sleep behavioral disorder. The large amount of experimental data has been obtained that deal with neurochemical mechanisms that are responsible for sleep-related depression of various motoneuron groups. However, there is a disagreement regarding the outcome of these studies primarily due to the use of different animal models and approaches, as well as due to differences in quantification and interpretation of obtained results. In this study, we sought to apply the same calculation methodology in order to uniformly quantify and compare the relative contribution of excitatory or inhibitory inputs to the decrease of excitability of different motoneuronal pools during REM and/or non-REM sleep. We analyzed only published quantitative data that were obtained by using receptor antagonists or chemogenetic approach to block receptors or silence neuronal populations. The outcomes of this analysis highlight the differences in the neurotransmitter mechanisms of sleep-related motoneuron depression between different motoneuronal pools and demonstrate the consistency of these mechanisms for hypoglossal motoneurons among various animal models.
Highlights
The decrease of upper airway motoneuron excitability during rapid eye movement (REM) sleep and non-REM (NREM) sleep is a major neurological cause of obstructive sleep apnea (OSA), which is recognized as a severe and growing sleep disorder [1, 2]
Intracellular parameters of motoneurons were measured during NREM sleep in control (Ncon) and after the antagonist (Nant) and during REM sleep before (Rcon) and after the antagonist (Rant)
(3) Our analysis suggests the following: (a) both GABA and glycine may play a role during NREM sleep-induced depression of hypoglossal motoneurons (HM) [19, 25, 27, 28, 35, 47, 48]; (b) Noradrenergic excitatory input plays a major role in HM
Summary
The decrease of upper airway motoneuron excitability during rapid eye movement (REM) sleep and non-REM (NREM) sleep is a major neurological cause of obstructive sleep apnea (OSA), which is recognized as a severe and growing sleep disorder [1, 2]. The insufficient inhibition of spinal motoneurons during REM sleep causes REM sleep behavioral disorder [3,4,5]. The OSA is associated with excessive daytime sleepiness, cognitive impairements and decreased quality of life [6,7,8,9,10,11,12]. The OSA is linked to hypertension [12,13,14,15,16] and the increased risk of stroke [17].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
