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.
Tsuneki
H
H
Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Toyama Medical and Pharmaceutical University, Japan.
Dezaki
K
K
Kimura
I
I
D000157:Aconitine / Q000031:analogs & derivatives* / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D008297:Male; D051379:Mice; D009045:Motor Endplate / Q000187:drug effects* / Q000378:metabolism; D009469:Neuromuscular Junction / Q000187:drug effects; D011978:Receptors, Nicotinic / Q000187:drug effects*; D013997:Time Factors
D011978:Receptors, Nicotinic; C054634:methyllycaconitine; D002118:Calcium; D000157:Aconitine