Nanoscale remodeling of sodium channels in the cardiac transverse tubules contributes to aberrant calcium release in a Scn1a haploinsufficient mouse

Mice harboring a haploinsufficiency in Scn1a (the gene encoding Nav1.1) present with a paradoxical increase in persistent Na+ current (INa). Further, Nav1.1+/- mice show an increased susceptibility to arrhythmia development and sudden unexplained death, though the mechanism remains poorly understood. To address this, we examined functional NaV distribution in cardiomyocytes.