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Sustained membrane potential depolarization can prevent repeated action potentials because voltage-dependent ion-channel inactivation leaves too few available sodium channels. This differs from a reduced response to a passive current step: active Hodgkin-Huxley model dynamics and recovery from inactivation are essential to the mechanism.

A node of Ranvier is a short gap between adjacent myelin sheaths along an axon. Its exposed cell membrane contains a high density of voltage-dependent sodium channels, allowing an action potential to be regenerated after local electric current has spread beneath the preceding sheath. Repetition of this arrangement supports saltatory conduction.^[ref]

A node is not a gap in the axon itself. The interior remains continuous while the surrounding insulation is interrupted. This distinction explains how current can travel between electrically excitable regions without crossing a synapse.

A sodium channel is an ion channel that preferentially conducts sodium ions. In a voltage-gated sodium channel, changes in membrane potential control opening and inactivation. Under usual neuronal conditions, opening permits inward current that promotes depolarization, recruiting more voltage-gated sodium channels during the rising phase of an action potential. ^[ref]

An illustrative current relation is $I_{Na}=g_{Na}(V-E_{Na})$, with an explicitly chosen sign convention. Even a large conductance produces little net current near the sodium reversal potential. Channel availability, opening and ionic driving force are therefore distinct. Inactivation also differs from merely closing a resting activation gate: recovery depends on the preceding voltage history.