= Neuronal refractory period
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 $h$ restores <sodium> availability and relaxation of $n$ reduces <potassium> <electrical conductance>. Closed but available channels differ from inactivated channels: opening and recovery from <ion-channel inactivation> are different processes.<Neuronal Dynamics: From Single Neurons to Networks and Models of Cognition by Wulfram Gerstner and others/2.2 Hodgkin-Huxley Model>[§2.2.1, Activation and De-inactivation; §2.2.3, Figure 2.6 and Ion channel dynamics during spike generation]{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.
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