Abstract
The second phase of Ca 2+ transients (aequorin luminescence) which was not accompanied by twitch tensions were generated by 0.3 μM neostigmine in indirectly-stimulated diaphragm muscles of mice. This phase was dependent on external [Ca 2+] 0, was inhibited by a low concentration of (+)-tubocurarine (+)-TC; 0.013–0.13 μM) or pancuronium (Panc; 0.034–0.14 μM), and was not inhibited by atropine (3 μM) or nitrendipine (10 μM). These results suggest that nicotinic acetylcholine receptor highly sensitive to (+)-TC may stimulate Ca 2+ influx through receptor-operated Ca 2+ channels.
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