Sodium channel subtypes in the rat display functional differences in the presence of veratridine.

The alkaloid neurotoxin veratridine has the unique property of functionally distinguishing sodium channel subtypes in the rat through differences in single channel conductances, channel substates and probability of channel opening. Veratridine-activated cardiac sodium channels from rat ventricular muscle displayed a single channel conductance of 8.4 pS with no evidence of subconductance states or channel subtypes. Rat skeletal muscle sodium channels displayed both high (8.5 pS) and low conductance (4.7 pS) openings as well as a lower probability of opening (approximately 50%) at depolarized potentials than shown with brain or cardiac sodium channels (90-95%). Rat brain veratridine-activated sodium channels displayed primarily subconductance states at depolarized potentials (3-6 pS) and full conductance of approximately 9.5 pS at hyperpolarized potentials.