The second phase of Ca2+ transients (aequorin luminescence) which was not accompanied by twitch tensions were generated by 0.3 microM neostigmine in indirectly-stimulated diaphragm muscles of mice. This phase was dependent on external [Ca2+]o, was inhibited by a low concentration of (+)-tubocurarine (+)-TC; 0.013-0.13 microM) or pancuronium (Panc; 0.034-0.14 microM), and was not inhibited by atropine (3 microM) or nitrendipine (10 microM). These results suggest that nicotinic acetylcholine receptor highly sensitive to (+)-TC may stimulate Ca2+ influx through receptor-operated Ca2+ channels.
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