Voltage-gated sodium channel

Class

Topical sodium-channel blocker

Voltage-gated sodium channels are membrane proteins that open briefly when a neuron's membrane depolarizes, allowing a rapid influx of sodium ions that generates the rising phase of the action potential, the electrical signal by which nerve and muscle cells communicate. Because repetitive, high-frequency firing of neurons underlies seizures and certain pain states, drugs that reduce sodium channel availability during periods of sustained depolarization can dampen this excessive activity without abolishing normal, low-frequency signaling. This selective effect on pathologically active cells is called use-dependent or state-dependent block, and it is the shared mechanism behind a large family of anticonvulsant medicines. By stabilizing the inactivated state of the channel, these agents raise the threshold required to sustain rapid firing, which helps prevent the synchronized neuronal discharges characteristic of epileptic seizures. Related channel subtypes also contribute to pain signal transmission in peripheral nerves, making this mechanism relevant to certain neuropathic pain conditions as well. Because sodium channels exist in many tissues, including heart and skeletal muscle, the therapeutic goal is to achieve enough central or peripheral neuronal blockade to control seizures or pain while minimizing effects on channels that maintain normal cardiac rhythm and motor function.