Voltage-gated sodium channel (Nav channel)

Voltage-gated sodium channels are integral membrane proteins that form selective pores for the rapid influx of Na^+ ions across cell membranes in response to changes in membrane potential. They are essential for the initiation and propagation of action potentials in excitable cells such as neurons, muscle cells, and cardiomyocytes. The canonical structure consists of a large α-subunit forming the pore—composed of four homologous domains each with six transmembrane segments—and auxiliary β-subunits that modulate function and localization. There are nine main mammalian isoforms (Nav1.1–Nav1.9), each with distinct tissue distributions and physiological roles; for example, Nav1.5 is predominant in heart tissue while Nav1.7–Nav1.9 are key in peripheral nerves involved in pain transmission. These channels can be pharmacologically classified as tetrodotoxin-sensitive or -resistant types depending on their sensitivity to this neurotoxin.\n\nDysfunction or altered expression of voltage-gated sodium channels is implicated in a range of diseases including epilepsy, chronic pain syndromes, cardiac arrhythmias, and certain myopathies. Drugs targeting these channels include anticonvulsants like carbamazepine (which stabilizes the inactive state), local anesthetics like lidocaine (which block conduction), as well as antiarrhythmic agents used clinically for heart rhythm disorders.

Other names

Sodium ion channelVoltage-dependent sodium channelVoltage-sensitive sodium channelNav (for individual subtypes, e.g., Nav1.7)

Blockade of voltage-gated sodium channels to reduce neuronal excitability or conduction