Abstract
Calcium has been suggested as the second messenger link between skeletal muscle activity and AChR gene expression and synthesis. We have compared the concentrations of the Ca2+ channel antagonists D600 and nisoldipine needed both to block Ca2+ uptake into cultured myotubes and to increase AChR expression. The good correspondence between these two measurements and the use of the highly specific Ca2+ channel antagonist nisoldipine strengthens the hypothesis that AChR expression is regulated by levels of intracellular Ca2+.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / pharmacology
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Animals
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Bungarotoxins / metabolism*
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Calcium / metabolism
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Calcium Channel Blockers / pharmacology*
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Cells, Cultured
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Chick Embryo
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Gallopamil / pharmacology*
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Kinetics
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Muscles / metabolism*
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Nifedipine / analogs & derivatives
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Nifedipine / pharmacology
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Nisoldipine
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Receptors, Cholinergic / drug effects
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Receptors, Cholinergic / metabolism*
Substances
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Bungarotoxins
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Calcium Channel Blockers
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Receptors, Cholinergic
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Gallopamil
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Nisoldipine
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3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester
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Nifedipine
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Calcium