ArticleCommunications biology2018
Alcohol reduces muscle fatigue through atomistic interactions with nicotinic receptors.
Article in Communications biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Cryo-EM Structures of Alcohol Oxidase Isozymes Reveal Structural Determinants of Cofactor Variation and Enzymatic Activity in Ogataea methanolica.Microbial biotechnology · 2026Article
- Alcohol-Mediated Skeletal Muscle Adaptations and Their Impact on Comorbidities.The American journal of pathology · 2026Review
- Synaptic Effects Induced by Alcohol.Current topics in behavioral neurosciences · 2025Review
- Alcohol and Skeletal Muscle in Health and Disease.Alcohol research : current reviews · 2023Review
- Embryonic ethanol exposure disrupts craniofacial neuromuscular integration in zebrafish larvae.Frontiers in physiology · 2023Article
- Alcohol reduces muscle fatigue through atomistic interactions with nicotinic receptors.Communications biology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 6 institutions in 2 countries.
Funding
Abstract
Alcohol consumption affects many organs and tissues, including skeletal muscle. However, the molecular mechanism of ethanol action on skeletal muscle remains unclear. Here, using molecular dynamics simulations and single channel recordings, we show that ethanol interacts with a negatively charged amino acid within an extracellular region of the neuromuscular nicotinic acetylcholine receptor (nAChR), thereby altering its global conformation and reducing the single channel current amplitude. Charge reversal of the negatively charged amino acid abolishes the nAChR-ethanol interaction. Moreover, using transgenic animals harboring the charge-reversal mutation, ex vivo measurements of muscle force production show that ethanol counters fatigue in wild type but not homozygous αE83K mutant animals. In accord, in vivo studies of motor coordination following ethanol administration reveal an approximately twofold improvement for wild type compared to homozygous mutant animals. Together, the converging results from molecular to animal studies suggest that ethanol counters muscle fatigue through its interaction with neuromuscular nAChRs.
Identifiers
What OpenQuestion holds
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.