Anticonvulsants modify inactivation but not activation processes of sodium channels in Myxicola axons.
The effects of pronase and the anticonvulsant drugs diphenylhydantoin, bepridil, and sodium valproate on fast and slow Na+ inactivation were examined in cut-open Myxicola giant axons with loose patch-clamp electrodes applied to the internal surface. Pronase completely eliminated fast Na+ inactivation without affecting the kinetics of Na+ activation or the maximum Na+ conductance. The time and voltage dependences of slow inactivation following pronase treatment were identical to those measured before enzyme application in the same axons. All three anticonvulsants slowed the time course of recovery from fast Na+ inactivation in untreated axons, and shifted the steady-state fast inactivation curve in the hyperpolarizing direction along the voltage axis. Anticonvulsants enhanced steady-state slow inactivation and retarded recovery from slow inactivation in both untreated and pronase-treated axons. Although some quantitative differences were seen, the order of potency of the anticonvulsants on slow Na+ inactivation was the same as that for recovery from fast inactivation.
D000818:Animals; D000927:Anticonvulsants / Q000494:pharmacology*; D001369:Axons / Q000187:drug effects / Q000502:physiology; D015764:Bepridil; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology*; D010672:Phenytoin / Q000494:pharmacology; D011077:Polychaeta; D011402:Pronase / Q000494:pharmacology; D011759:Pyrrolidines / Q000494:pharmacology; D012964:Sodium / Q000378:metabolism*; D014635:Valproic Acid / Q000494:pharmacology
D000927:Anticonvulsants; D007473:Ion Channels; D011759:Pyrrolidines; D014635:Valproic Acid; D010672:Phenytoin; D015764:Bepridil; D012964:Sodium; D011402:Pronase