Voltage-Gated Sodium Channel (VGSC)

Voltage-gated sodium channels (VGSCs or NaV channels) are essential transmembrane proteins that enable the rapid influx of sodium ions (Na⁺) into excitable cells, such as neurons, muscle cells, and cardiac myocytes. This influx is critical for the initiation and propagation of action potentials—electrical signals that underlie nerve impulses, muscle contraction, and heartbeats. The core functional unit is a large alpha (α) subunit which forms the ion-conducting pore. Accessory beta (β) subunits associate with α subunits to modulate channel kinetics, voltage dependence, localization, and cell-surface expression. There are multiple VGSC isoforms encoded by different genes (e.g., SCN1A-SCN11A), each subtype has unique gating properties suited to its physiological context. Mutations or dysregulation can cause diseases such as epilepsy, chronic pain syndromes, periodic paralysis disorders, or cardiac arrhythmias. VGSCs are major drug targets.

Other names

NaV channelSodium channelVoltage-sensitive sodium channel

Drugs block the channel pore or modify gating behavior, preventing Na⁺ influx and inhibiting action potential generation.