Voltage-gated sodium channel

A membrane protein that opens in response to changes in membrane voltage, allowing sodium ions to enter excitable cells and help generate electrical impulses.

Action potential: A rapid, transient change in a cell’s membrane voltage that carries electrical signals. Sodium-channel opening produces the rising phase of many action potentials.
Cell membrane: A lipid-based boundary that separates a cell’s interior from its surroundings. The channel is embedded in this barrier and spans it.
Nav1.7: A voltage-gated sodium-channel subtype encoded by the SCN9A gene and expressed prominently in peripheral pain-sensing neurons. Its activity strongly influences whether nociceptors initiate pain signals.
Alan Hodgkin: A British physiologist who helped establish the ionic basis of the action potential. His voltage-clamp work helped reveal voltage-dependent sodium currents.
Dravet syndrome: A severe developmental and epileptic encephalopathy that often begins with prolonged seizures in infancy. Many cases result from loss-of-function variants in SCN1A, which encodes Nav1.1.
Voltage sensor: A protein region that detects changes in electrical potential across a membrane. Charged parts of this channel domain move when membrane voltage changes.
Membrane potential: The electrical voltage difference between the inside and outside of a cell. Changes in this voltage control channel opening.
Nav1.5: The principal voltage-gated sodium-channel subtype responsible for rapid depolarization in working heart muscle. Its current helps conduct electrical impulses through the myocardium.
Andrew Huxley: A British physiologist who developed quantitative models of nerve action potentials with Alan Hodgkin. Their experiments separated sodium and potassium contributions to electrical signals.
Erythromelalgia: A rare disorder marked by episodic burning pain, redness, and warmth, usually in the extremities. Some inherited cases arise from gain-of-function variants in the Nav1.7 channel.

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