Methyl-β-cyclodextrin (0.1 mM) reduced resting potential of muscle fibers and abolished local endplate membrane hyperpolarization in rat diaphragm. This effect was associated with selective reduction of electrogenic activity of α2-isoform of Na,K-ATPase without changes in the level of intracellular acetylcholine. Experiments with cholesterol marker filipin showed that methyl-β-cyclodextrin in this dose induced cholesterol translocation from lipid rafts to liquid phase of the membrane without its release into extracellular space. This modification of lipid rafts by methyl-β-cyclodextrin presumably impaired the mechanism maintaining electrogenesis in endplates mediated by modulation of Na,K-ATPase by non-quantum acetylcholine. Cholesterol can serve as a molecular component of this mechanism.
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Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 158, No. 9, pp. 275–278, September, 2014
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Kravtsova, V.V., Petrov, A.M., Vasil’ev, A.N. et al. Role of Cholesterol in the Maintenance of Endplate Electrogenesis in Rat Diaphragm. Bull Exp Biol Med 158, 298–300 (2015). https://doi.org/10.1007/s10517-015-2745-8
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DOI: https://doi.org/10.1007/s10517-015-2745-8