Neuronal refractory period Created 2026-10-13 Updated 2026-10-14
A neuronal refractory period is the change in excitability following an action potential: recent firing changes whether, and how readily, a neuron can fire again. The absolute neuronal refractory period prevents a second regenerative action potential; during the relative neuronal refractory period, some stimuli that work after full recovery still fail. These are useful distinctions, but their durations are not universal constants. The preparation, temperature, starting membrane potential, stimulation protocol and criterion for detecting an action potential must accompany a measured interval.
The mechanism continues the opposing sodium and potassium electric currents described under action potential and the Hodgkin-Huxley model. After a spike, ion-channel inactivation leaves fewer sodium-selective voltage-gated ion channels available for regenerative depolarization, while persisting potassium electrical conductance opposes that depolarization. In the Hodgkin-Huxley model, recovery of restores sodium availability and relaxation of reduces potassium electrical conductance. Closed but available channels differ from inactivated channels: opening and recovery from ion-channel inactivation are different processes.[ref]
This short memory matters for spike trains: a stimulus-only Poisson process can predict very short interspike intervals that a refractory neuron cannot produce. Neuronal paired-pulse recovery makes that memory visible. The phenomenological paired-pulse recovery example below separates a chosen recovery rule, pulse strength and event readout; refractory limits on neuronal firing then shows why an absolute bound is not a prediction of sustained firing rate.
During a relative neuronal refractory period, another action potential is possible, but incomplete recovery changes the excitation needed to obtain it. Remaining sodium ion-channel inactivation and elevated potassium electrical conductance both matter. A hyperpolarization after an action potential can increase the voltage excursion needed for firing, while extra electrical conductance can drain an injected pulse faster. Thus a single fixed neuronal firing threshold measured from the instantaneous voltage misses relevant state variables.[ref]
Recovery can depend on earlier spikes as well as the last one; the Hodgkin-Huxley model and neural adaptation provide richer histories than an imposed reset. A fixed hold in a leaky integrate-and-fire model is a useful simplification with a specified domain, rather than a complete explanation of a relative neuronal refractory period.[ref]