Journal
BULLETIN OF EXPERIMENTAL BIOLOGY AND MEDICINE
Volume 158, Issue 3, Pages 298-300Publisher
SPRINGER
DOI: 10.1007/s10517-015-2745-8
Keywords
cholesterol; lipid rafts; Na,K-ATPase; acetylcholine
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Funding
- St. Petersburg State University [1.50.1621.2013, 1.38.231.2014]
- Russian Foundation for Basic Researches [13-04-00973a, 14-04-00094a]
- [MK-108.2014.4]
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Methyl-beta-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 alpha 2-isoform of Na,K-ATPase without changes in the level of intracellular acetylcholine. Experiments with cholesterol marker filipin showed that methyl-beta-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-beta-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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