Voltage-gated sodium channels (Na_V) are essential for the generation of action potentials and for cell excitability.¹ Na_V channels are activated in response to depolarization and selectively allow flow of Na⁺ ions. To date, nine Na_V α subunits have been cloned and named Na_V1.1-Na_V1.9.^4-5 The Na_V channels are classified into two groups according to their sensitivity to Tetrodotoxin (TTX): TTX-sensitive (Na_V1.1, Na_V1.2, Na_V1.3, Na_V1.4, Na_V1.6 and Na_V1.7) and TTX-resistant (Na_V1.5, Na_V1.8 and Na_V1.9).^2-3

Mammalian sodium channels are heterotrimers, composed of a central, pore-forming α subunit and two auxiliary β subunits. The 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 sodium channels in adult skeletal muscle have only the β₁ subunit.^6,7

Na_V1.2, also known as SCN2A, is primarily expressed in the central nervous system (CNS) and is localized in unmyelinated or premyelinated axons and dendrites. Mutations in the Na_V1.2 channel have been identified in different types of epilepsy.