A study of the effects of (+)-methysticin on sodium channels of isolated neurons from theCA1 hippocampal area of rats showed that this drug considerably accelerabed the inactivation processes providing that the membrane potential was within the −80 to −20 mV range. When depolarization was further increased, the influence of methysticin on the rate of inactivation became much smaller. Hyperpolarization of the membrane removed inactivation. Methysticin (100 μM) intensively slowed down deinactivation and decreased the dependence of the rate of this process on the membrane potential. The effect of methysticin on inactivation kinetics results in considerable shifts of the neurons' excitability; this probably underlies neuroprotective effects of this drug manifested in the model of focal cerebral ischemia in rats and mice.