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  • Title: [Slow Ca2+ (RAMIC) mobilization operated by postsynaptic neuronal nicotinic receptor regulates synaptic function at the mouse neuromuscular junction].
    Author: Dezaki K, Tsuneki H, Kimura I.
    Journal: Nihon Yakurigaku Zasshi; 1997 Oct; 110 Suppl 1():114P-119P. PubMed ID: 9503417.
    Abstract:
    We have found that non-contractile slow Ca2+ mobilization (RAMIC; Receptor-Activity Modulating Intracellular Ca2+) is generated by motor nerve stimulation with anti-cholinesterase at the skeletal muscle, and desensitizes muscle nicotinic receptor (nAChR). To confirm this Ca2+ mobilization without anti-cholinesterase, acetylcholine (ACh) was locally applied by N2-gas pressure onto endplate region at the mouse phrenic nerve-diaphragm muscle preparation. ACh (0.1-3 mM, 20 microliters) elicited bi-phasic elevation of [Ca2+]i (fast and slow Ca2+ mobilization measured as Ca(2+)-aequorin luminescence) in muscle cells. The peak amplitude of slow Ca2+ mobilization (not accompanied by contraction) was increased by ACh concentration-dependently, whereas that of fast component (accompanied by contraction) reached a maximum response at a lower concentration of ACh. The slow Ca2+ mobilization was blocked by lower concentrations of competitive nAChR antagonists which did not affect the fast Ca2+ transients. Moreover, the slow Ca2+ signal was selectively depressed by a neuronal nAChR antagonist methyllycaconitine. Neither Ca2+ channel blockers nor a Na+ channel blocker tetrodotoxin prevented the generation of the slow Ca2+ mobilization. These results suggest that RAMIC is mobilized through postsynaptic neuronal nAChR subtype to desensitize muscle nAChR at the neuromuscular junction.
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