title: Homeostatic regulation through GABA and acetylcholine muscarinic receptors of motor trigeminal neurons following sleep deprivation.
abstract: Muscle tone is regulated across sleep-wake states, being maximal in waking, reduced in slow wave sleep (SWS) and absent in paradoxical or REM sleep (PS or REMS). Such changes in tone have been recorded in the masseter muscles and shown to correspond to changes in activity and polarization of the trigeminal motor 5 (Mo5) neurons. The muscle hypotonia and atonia during sleep depend in part on GABA acting upon both GABAAand GABABreceptors (Rs) and acetylcholine (ACh) acting upon muscarinic 2 (AChM2) Rs. Here, we examined whether Mo5 neurons undergo homeostatic regulation through changes in these inhibitory receptors following prolonged activity with enforced waking. By immunofluorescence, we assessed that the proportion of Mo5 neurons positively stained for GABAARs was significantly higher after sleep deprivation (SD, ~65%) than sleep control (SC, ~32%) and that the luminance of the GABAAR fluorescence was significantly higher after SD than SC and sleep recovery (SR). Although, all Mo5 neurons were positively stained for GABABRs and AChM2Rs (100%) in all groups, the luminance of these receptors was significantly higher following SD as compared to SC and SR. We conclude that the density of GABAA, GABABand AChM2 receptors increases on Mo5 neurons during SD. The increase in these receptors would be associated with increased inhibition in the presence of GABA and ACh and thus a homeostatic down-scaling in the excitability of the Mo5 neurons after prolonged waking and resulting increased susceptibility to muscle hypotonia or atonia along with sleep.
authors.affiliation: Department of Neurology and Neurosurgery, McGill University, Montreal Neurological Institute, 3801 University Street, Montreal, QC, H3A 2B4, Canada.
authors.forename: Hanieh
authors.initials: H
authors.lastname: Toossi
authors.affiliation: Department of Neurology and Neurosurgery, McGill University, Montreal Neurological Institute, 3801 University Street, Montreal, QC, H3A 2B4, Canada.
authors.forename: Esther
authors.initials: E
authors.lastname: Del Cid-Pellitero
authors.affiliation: Department of Neurology and Neurosurgery, McGill University, Montreal Neurological Institute, 3801 University Street, Montreal, QC, H3A 2B4, Canada. barbara.jones@mcgill.ca.
authors.forename: Barbara E
authors.identifier: http://orcid.org/0000-0001-9985-3860
authors.initials: BE
authors.lastname: Jones
mesh_terms: D000109:Acetylcholine / Q000378:metabolism; D000818:Animals; D002452:Cell Count; D004569:Electroencephalography; D005786:Gene Expression Regulation / Q000502:physiology; D006706:Homeostasis / Q000502:physiology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009046:Motor Neurons / Q000502:physiology*; D018079:Receptors, GABA / Q000378:metabolism*; D011976:Receptors, Muscarinic / Q000378:metabolism*; D012892:Sleep Deprivation / Q000473:pathology*; D013997:Time Factors; D066266:Trigeminal Motor Nucleus / Q000473:pathology*; D014851:Wakefulness / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D018079:Receptors, GABA; D011976:Receptors, Muscarinic; D005680:gamma-Aminobutyric Acid; D000109:Acetylcholine
keywords: AChM2; GABAA; GABAB; Mice; Muscle atonia; Waking