Neuronal nicotinic receptor operates slow Ca2+ mobilization at mouse muscle endplate

The contribution to neuromuscular functions by neuronal nicotinic acetylcholine receptor (nAChR) expressed at skeletal muscle endplate was investigated using intracellular Ca2+ measurements. A neuronal nAChR blocker, methyllycaconitine (MLA), depressed non-contractile Ca2+ mobilization without affecting muscle nAChR activity in nerve-stimulated mouse diaphragm muscle, after cholinesterase inhibition. Confocal imaging demonstrates that the MLA-sensitive Ca2+ mobilization also occurred at the endplate in single flexor digitorum brevis muscle cells as the slow component of two-phasic Ca2+ elevation after the prolonged nicotinic stimulation. A monoclonal antibody to alpha 1 subunit of muscle nAChR depressed the fast but not the slow component. Thus, muscle neuronal-nAChR can induce the localized rise of Ca2+ at the postjunctional sites.