Abstract
Local application of acetylcholine (ACh; 0.3 mM, 20 μl) elicited bi-phasic elevation of intracellular Ca 2+ concentrations (contractile fast and non-contractile slow Ca 2+ signal measured as aequorin luminescence) in diaphragm muscle preparation. A neuronal nicotinic antagonist methyllycaconitine (MLA; 0.01–1 μM), which did not affect the fast Ca 2+ transients and twitch tension, concentration-dependently depressed only the slow Ca 2+ component. Ca 2+ channel blockers, Cd 2+ (200 μM), nitrendipine (1 μM), verapamil (1 μM) and diltiazem (1 μM), or a Na + channel blocker tetrodotoxin (TTX; 0.1 μM) failed to prevent the generation of slow Ca 2+ response. Perfusion of ACh (1 μM) to isolated single skeletal (flexor digitorum brevis) muscle cells pretreated with TTX (0.1 μM) also elicited a slow Ca 2+ signal measured as confocal imaging with a fluorescent dye, fluo-3, at the endplate region. MLA (1 μM) antagonized against the ACh perfusion-elicited slow Ca 2+ signal. Perfusion of choline (1 mM), a neuronal nicotinic agonist, also elicited the MLA-sensitive slow Ca 2+ signal. These results strongly suggest that the ACh-induced slow Ca 2+ signal reflects Ca 2+ entry through a postsynaptic MLA-sensitive neuronal nicotinic Ach receptor subtype at the neuromuscular junction.
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