SCN7A, also known as Na_X, Nav2.1 or Nav2.3, is an atypical member of the SCNA family of voltage-dependent sodium channels, that includes nine mammalian members: Nav1.1 through Nav1.9.

As its name implies, SCN7A was initially identified as a new member of the Nav channel family. However, atypical sequence features, namely fewer positive charged residues in the S4 voltage sensor domain than other sodium channels, and the inability to record voltage-activated sodium currents, raised speculation that this channel might have distinct physiological roles. ^1,2

Indeed, a role of SCN7A as a sensor of extracellular sodium concentrations, has been described.

SCN7A is expressed both in the central nervous system and in peripheral organs. In the brain, SCN7A expression appears in both neurons and glia cells. Experiments with SCN7A knockout mice, showed that SCN7A might function as an extracellular sodium sensor. Knockout mice demonstrated abnormal saline-intake behaviour under conditions of water deprivation, as well as abnormal blood pressure changes after salt intake. ^2,3,4

In addition, expression of SCN7A in epithelial tissues has been linked to epithelial homeostasis following injury. Water loss following skin disorders or injury, will result in an increase in extracellular sodium concentration and hence, will be able to stimulate SCN7A function. Indeed, blocking of SCN7A function in epithelial tissues in animal models, showed a decrease in scarring and atopic dermatitis–like symptoms. ^2,5,6