Slow sodium channel inactivation in mammalian muscle: a possible role in regulating excitability.

Sodium currents were recorded in rat fast and slow twitch muscle fibers. Changes in the membrane potential around the resting potential produced slow changes in the sodium current amplitude due to alterations of the slow inactivation process that was increased by steady depolarization and removed by prolonged hyperpolarization. In contrast, classical fast inactivation was not operative around the resting potential, and depolarizations of greater than 20 mV were required to close half of the channels by fast inactivation. Because slow inactivation is operative around the resting potential of mammalian muscle fibers, it may partially explain why small depolarizations, such as those that occur in some patients with periodic paralysis, can reduce excitability.