GNA

gNa is the sodium conductance of a cell’s membrane, representing the ease with which sodium ions cross the membrane through voltage‑gated sodium channels. In biophysical models, gNa denotes a time- and voltage-dependent conductance and is a key component of the sodium current.

In the Hodgkin–Huxley framework, gNa can be written as gNa(t) = GNa · m^3 · h, where GNa is the maximum or peak sodium conductance, and m and h are gating variables that reflect activation and inactivation of the channels. Upon depolarization, activation gates (m) rapidly open to increase gNa, while inactivation gates (h) close more slowly, causing gNa to fall despite continued depolarization. The sodium reversal potential, ENa, is typically around +50 to +60 mV, driving an inward current that underlies the rapid upstroke of the action potential.

Physiologically, gNa determines how quickly a neuron can initiate and propagate action potentials. It varies across cell types and conditions, and is influenced by temperature, channel phosphorylation, and the lipid environment. Pharmacological agents and toxins that block or modify voltage-gated sodium channels effectively alter gNa.

Typical reference values are context-dependent; in the classical Hodgkin–Huxley model of the squid giant axon, GNa is about 120 mS/cm^2, with ENa near +50 mV. Across neurons, gNa is measured experimentally via voltage-clamp techniques and can be modulated by development, disease, or pharmacological intervention.