This illustration further conceptualizes the complex role of voltage gates sodium and potassium channels in neuronal excitability. There are 4 states of the voltage-gated channel opening and closing as it relates to the generation of an action potential: resting, depolarizing, repolarizing, and hyperpolarization. See A-D. The diagram conceptualizes what is occurring at the membrane level that corresponds to the action potential. One sees the sodium channel open correlating to the depolarizing phase. Repolarization occurs with closure of the inactivating gate and activating gate m. Potassium influx correlates with hyperpolarization stabilizing the membrane and bringing the system back to the resting state. Carbamazepine, felbamate lacosamide, lamotrigine oxcarbaxepine, phenytoin, rufinamide, topiramate, zonisamide, and valproic acid all modulate this channel to some degree. Lacosamide appears to modulate the complex slightly differently from the other sodium channels. Ezogabine appears to modulate the system at the potassium channel. Understanding the complexity of this channel helps to better demonstrate how varying antiepileptic drugs functioning at various parts of the channel may have complementary benefits. This has yet to be proven clinically.
Reprinted from Webanatomy.3