English
 
User Manual Privacy Policy Disclaimer Contact us
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Alcohol reduces muscle fatigue through atomistic interactions with nicotinic receptors

MPS-Authors
/persons/resource/persons214538

Noori,  HR
Research Group Neuronal Convergence, Max Planck Institute for Biological Cybernetics, Max Planck Society;
Max Planck Institute for Biological Cybernetics, Max Planck Society;

/persons/resource/persons214898

Bagher Oskouei,  M
Max Planck Institute for Biological Cybernetics, Max Planck Society;
Research Group Neuronal Convergence, Max Planck Institute for Biological Cybernetics, Max Planck Society;

Fulltext (public)
There are no public fulltexts available
Supplementary Material (public)
There is no public supplementary material available
Citation

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.


Cite as: http://hdl.handle.net/21.11116/0000-0002-512F-F
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.