Voltage-gated sodium channels (Nav) are essential for the generation of action potentials and for cell excitability.1 Nav channels are activated in response to depolarization and selectively allow flow of Na+ ions. To date, nine Nav α subunits have been cloned and named Nav1.1-Nav1.9. The Nav channels are classified into two groups according to their sensitivity to Tetrodotoxin (TTX): TTX-sensitive (Nav1.1, Nav1.2, Nav1.3, Nav1.4, Nav1.6 and Nav1.7) and TTX-resistant (Nav1.5, Nav1.8 and Nav1.9). Mammalian Na+ channels are heterotrimers, composed of a central pore-forming α subunit and two auxiliary β subunits. Expression of the α subunit isoform is developmentally regulated and tissue specific. Sodium channels in the adult central nervous system and heart contain β1 through β4 subunits, whereas Na+ channels in adult skeletal muscle have only the β1 subunit.Nav1.2 is primarily expressed in the central nervous system (CNS) and is localized in unmyelinated or premyelinated axons and dendrites. Mutations in the Nav1.2 channel have been identified in different types of epilepsy.
