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  Alcohol reduces muscle fatigue through atomistic interactions with nicotinic receptors

Noori, H., Mücksch, C., Vengeliene, V., Schönig, K., Takahashi, T., Mukhtasimov, N., et al. (2018). Alcohol reduces muscle fatigue through atomistic interactions with nicotinic receptors. Communications Biology, 1: 159, pp. 1-11. doi:10.1038/s42003-018-0157-9.

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https://www.nature.com/articles/s42003-018-0157-9.pdf (Verlagsversion)
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 Urheber:
Noori, HR1, 2, Autor           
Mücksch, C, Autor
Vengeliene, V, Autor
Schönig, K, Autor
Takahashi, TT, Autor
Mukhtasimov, N, Autor
Bagher Oskouei, M1, 2, Autor           
Mosqueira, M, Autor
Bartsch, D, Autor
Fink, H, Autor
Urbassek, HM, Autor
Spanagel, R, Autor
Sine, SM, Autor
Affiliations:
1Research Group Neuronal Convergence, Max Planck Institute for Biological Cybernetics, Max Planck Society, ou_2528694              
2Max Planck Institute for Biological Cybernetics, Max Planck Society, ou_1497794              

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 Zusammenfassung: 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.

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 Datum: 2018-10
 Publikationsstatus: Online veröffentlicht
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 Identifikatoren: DOI: 10.1038/s42003-018-0157-9
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Titel: Communications Biology
Genre der Quelle: Zeitschrift
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Ort, Verlag, Ausgabe: -
Seiten: - Band / Heft: 1 Artikelnummer: 159 Start- / Endseite: 1 - 11 Identifikator: ISSN: 2399-3642