Voltage-gated Na⁺ channels (Na_V) are responsible for myocardial conduction and maintenance of the cardiac rhythm and are essential for the generation of action potentials and cell excitability.¹ Dysfunction or disregulation of cardiac sodium channels can cause several disorders, including cardiac arrhythmias.

The majority of Na⁺ channels in the mammalian heart are Tetrodotoxin (TTX)-insensitive Na_V1.5.²

The putative structure of Na_V1.5 consists of four homologous domains (I-IV), each containing six transmembrane segments (S1-S6). Mutations in the C-terminus of Na_V1.5 were described in connection to Long QT syndrome and Brugada syndrome.^1-2 Recent data have demonstrated selective expression of Na_V1.5 in the mouse central nervous system and implicated a role for Na_V1.5 in the physiology of the central nervous system.¹