A topic in the Open Knowledge Graph — a free, open map of 15,290 topics and the order to learn them in.
Depolarization (Na+ influx toward +30 mV), repolarization (K+ efflux, Na+ inactivation), afterhyperpolarization (delayed K+ closure). All-or-none: threshold crossed triggers full action potential.
You already know that neurons maintain a resting membrane potential around -70 mV, created by the unequal distribution of ions across the membrane and the selective permeability of leak channels. An action potential is what happens when that careful balance is temporarily overwhelmed — a brief, dramatic reversal of membrane polarity that propagates along the axon.
The initiating event is depolarization past threshold (~-55 mV). At that point, voltage-gated sodium channels snap open. Na+ ions, driven both by their concentration gradient (high outside) and by the negative membrane potential, flood inward. This influx rapidly drives the membrane potential from -70 mV up toward +30 mV — the peak of the action potential. The key word here is "all-or-none": if depolarization does not reach threshold, channels quickly close and the membrane recovers. If threshold is crossed, a self-reinforcing cascade (more depolarization → more channels open → more Na+ in) runs to completion every time, producing an identical spike regardless of how much the threshold was exceeded.
Repolarization begins almost immediately, driven by two concurrent changes. Voltage-gated Na+ channels transition into an inactivated state — different from their resting closed state — in which they cannot reopen. Simultaneously, voltage-gated K+ channels, which activate more slowly than Na+ channels, open and K+ flows outward down its electrochemical gradient. The combination of stopped Na+ influx and active K+ efflux drives the membrane potential back negative. Because K+ channels close with a slight delay, the membrane transiently overshoots resting potential, dipping to around -80 mV. This afterhyperpolarization is not a separate mechanism; it is simply the membrane following the K+ equilibrium potential until those slow K+ channels finally close.
The absolute refractory period — the window immediately after the spike during which no new action potential can be triggered — occurs because Na+ channels are inactivated and cannot respond to any stimulus. This has two important consequences: it ensures the action potential propagates in only one direction (the region behind the wavefront cannot be re-excited), and it sets a hard upper limit on how fast a neuron can fire. The relative refractory period that follows, when a suprathreshold stimulus *can* trigger a new spike, reflects the gradual recovery of Na+ channels from inactivation and the still-elevated K+ conductance.
Finally, note that the Na+/K+ ATPase pump does not meaningfully contribute to the immediate events of a single action potential — it operates on a much slower timescale. The ion movements during a single action potential are so small relative to the total ion concentration on each side that the gradients are essentially unaffected. The pump's job is maintenance over many spikes, not moment-to-moment restoration. This is a common misconception worth flagging: the action potential is driven by ion channels, not by the pump.