ArticleSleep2015
Postsynaptic inhibition of hypoglossal motoneurons produces atonia of the genioglossal muscle during rapid eye movement sleep.
Article in Sleep, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Desipramine Increases Genioglossus Activity and Reduces Upper Airway Collapsibility during Non-REM Sleep in Healthy Subjects.American journal of respiratory and critical care medicine · 2016Trial
- Mechanisms of upper airway muscle control in sleep reveal therapeutic targets for obstructive sleep apnea.American journal of respiratory cell and molecular biology · 2026Review
- Optical and pharmacological manipulation of hypoglossal motor nucleus identifies differential effects of taltirelin on sleeping tonic motor activity and responsiveness.Scientific reports · 2023Article
- GABA and glycine neurons from the ventral medullary region inhibit hypoglossal motoneurons.Sleep · 2020Article
- Measurement and State-Dependent Modulation of Hypoglossal Motor Excitability and Responsivity In-Vivo.Scientific reports · 2020Article
- Developmental nicotine exposure alters glycinergic neurotransmission to hypoglossal motoneurons in neonatal rats.Journal of neurophysiology · 2018Article
- Computational model of brain-stem circuit for state-dependent control of hypoglossal motoneurons.Journal of neurophysiology · 2018Article
- Catecholaminergic A1/C1 neurons contribute to the maintenance of upper airway muscle tone but may not participate in NREM sleep-related depression of these muscles.Respiratory physiology & neurobiology · 2017Article
- Homeostatic regulation through GABA and acetylcholine muscarinic receptors of motor trigeminal neurons following sleep deprivation.Brain structure & function · 2017Article
- Article
- The anatomical, cellular and synaptic basis of motor atonia during rapid eye movement sleep.The Journal of physiology · 2016Review
- Neural Control of the Upper Airway: Respiratory and State-Dependent Mechanisms.Comprehensive Physiology · 2016Review
- Revisiting Antagonist Effects in Hypoglossal Nucleus: Brainstem Circuit for the State-Dependent Control of Hypoglossal Motoneurons: A Hypothesis.Frontiers in neurology · 2015Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
STUDY
objectivesHypoglossal motoneurons were recorded intracellularly to determine whether postsynaptic inhibition or disfacilitation was responsible for atonia of the lingual muscles during rapid eye movement (REM) sleep.
designIntracellular records were obtained of the action potentials and subthreshold membrane potential activity of antidromically identified hypoglossal motoneurons in cats during wakefulness, nonrapid eye movement (NREM) sleep, and REM sleep. A cuff electrode was placed around the hypoglossal nerve to antidromically activate hypoglossal motoneurons. The state-dependent changes in membrane potential, spontaneous discharge, postsynaptic potentials, and rheobase of hypoglossal motoneurons were determined. ANALYSES AND
resultsDuring quiet wakefulness and NREM sleep, hypoglossal motoneurons exhibited spontaneous repetitive discharge. In the transition from NREM sleep to REM sleep, repetitive discharge ceased and the membrane potential began to hyperpolarize; maximal hyperpolarization (10.5 mV) persisted throughout REM sleep. During REM sleep there was a significant increase in rheobase, which was accompanied by barrages of large-amplitude inhibitory postsynaptic potentials (IPSPs), which were reversed following the intracellular injection of chloride ions. The latter result indicates that they were mediated by glycine; IPSPs were not present during wakefulness or NREM sleep.
conclusionsWe conclude that hypoglossal motoneurons are postsynaptically inhibited during naturally occurring REM sleep; no evidence of disfacilitation was observed. The data also indicate that glycine receptor-mediated postsynaptic inhibition of hypoglossal motoneurons is crucial in promoting atonia of the lingual muscles during REM sleep.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.