Voltage-Dependent Sodium Channel (Nav)

Voltage-dependent sodium channels are essential transmembrane proteins that enable the rapid influx of sodium ions (Na⁺) into cells in response to changes in membrane potential. This process is fundamental for the initiation and propagation of action potentials in excitable tissues such as nerves, muscles, and cardiac cells. The core functional unit is a large alpha (α) subunit that forms the ion-conducting pore. Accessory beta (β) subunits associate with α subunits to modulate gating properties and cellular localization but are not required for basic function. Nav channels cycle through three primary states: closed/resting, open/conducting, and inactivated. They mediate fast depolarization during action potentials. Multiple Nav channel isoforms exist (e.g., Nav1.7), encoded by different genes with tissue-specific expression patterns. Voltage-gated sodium channels are major drug targets; many local anesthetics, antiarrhythmics, anticonvulsants, and neurotoxins act by blocking or modifying Nav channel activity.

Other names

Voltage-gated Sodium ChannelSodium Channel

Blockage or modification of Nav channel activity, modulation of gating properties