Voltage-gated Na+ channels (NaV) 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 NaV1.5.2
The putative structure of NaV1.5 consists of four homologous domains (I-IV), each containing six transmembrane segments (S1-S6). Mutations in the C-terminus of NaV1.5 were described in connection to Long QT syndrome and Brugada syndrome.1-2 Recent data have demonstrated selective expression of NaV1.5 in the mouse central nervous system and implicated a role for NaV1.5 in the physiology of the central nervous system.1
