Key result
The dominant sodium current in the MCM1 cardiac cell line is insensitive to tetrodotoxin up to 100 microM and is reduced by agents that increase intracellular cAMP.
The MCM1 cardiac cell line exhibits a TTX-insensitive sodium current modulated by cAMP and blocked by desmethoxyverapamil, resembling embryonic sodium currents.
Provides murine model for cAMP-modulated TTX-resistant Na currents; leaves open human cardiac relevance.
The electrophysiological properties of a cardiac cell line (MCM1) originating from a transgenic mouse were characterized. The dominant current in these cells is a sodium current that is insensitive to concentrations of tetrodotoxin (TTX) up to 100 microM. It activates and inactivates rapidly with half-maximal activation at -40 mV and half-maximal inactivation at -79 mV. This sodium current is reduced by agents that increase intracellular adenosine 3',5'-cyclic monophosphate (cAMP) and activate cAMP-dependent protein kinase including isoproterenol, 8-bromo-cAMP, and isobutylmethylxanthine. The phenylalkylamine desmethoxyverapamil blocks the TTX-insensitive sodium current in MCM1 cells in both tonic and use-dependent fashion. Membrane depolarization enhances this block. It is proposed that the TTX-insensitive sodium current in these cells may be similar in origin to the embryonic type of TTX-insensitive sodium current described in other cardiac and skeletal muscle preparations.
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Sculptoreanu et al. (1992) studied this question. Tetrodotoxin (TTX) was evaluated on Electrophysiological properties of sodium current. The dominant sodium current in the MCM1 cardiac cell line is insensitive to tetrodotoxin up to 100 microM and is reduced by agents that increase intracellular cAMP.
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