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The action potential is a rapid, temporary change in membrane potential that allows neurons to transmit signals over long distances. It involves sequential opening of voltage-gated sodium channels (depolarization) followed by potassium channels (repolarization). The all-or-none principle means subthreshold stimuli don't trigger action potentials, creating a threshold for neural signaling.
Use voltage-clamp simulations to observe individual channel currents, then integrate to see whole-cell behavior. Graph the phases of the action potential against ion channel conductances to understand causation.
You already know that neurons sit at a resting membrane potential of approximately −70 mV, maintained by selective ion permeability and the Na⁺/K⁺-ATPase pump. You also know that voltage-gated ion channels open in response to changes in membrane potential — unlike the leak channels that maintain the resting state, these channels are sensitive to voltage and open or close based on it. The action potential is what happens when those channels interact in sequence.
When a stimulus depolarizes the membrane toward the threshold potential (roughly −55 mV), a critical number of voltage-gated sodium channels open. Na⁺ rushes in along its electrochemical gradient — high outside concentration, and a strongly negative interior that attracts positive ions. This inward Na⁺ current further depolarizes the membrane, which opens more sodium channels, which causes more depolarization. This positive feedback loop — called the Hodgkin cycle — drives the membrane potential from −70 mV to approximately +40 mV in less than a millisecond. This is the depolarization phase of the action potential, and once it begins above threshold, it goes to completion regardless of how large the original stimulus was. That is the all-or-none principle: either the threshold is reached and the full spike occurs, or nothing happens. A stimulus twice the threshold does not produce twice the action potential.
At the peak of depolarization, two processes converge to reverse it. Voltage-gated sodium channels enter an inactivated state — they close and cannot immediately reopen, no matter how depolarized the membrane is. Simultaneously, voltage-gated potassium channels (which open more slowly than sodium channels) reach full opening, allowing K⁺ to rush out along its electrochemical gradient. This outward K⁺ current brings the membrane back toward the potassium equilibrium potential, overshooting −70 mV slightly (the hyperpolarization phase, or afterhyperpolarization). During this period, the inactivated sodium channels cannot reopen, creating the absolute refractory period — the neuron physically cannot fire again, no matter how strong the stimulus.
Propagation exploits the local circuit currents generated by each spike. The depolarization at one segment of the axon causes current to flow into adjacent, still-resting membrane, which depolarizes that region above threshold and triggers its own action potential. Because the sodium channels in the just-fired region are inactivated, the wave can only travel in one direction — away from the initial site toward the terminal. This unidirectional propagation, combined with the all-or-none spike amplitude, means the signal arrives at the synaptic terminal with the same waveform it started with, regardless of distance. Neural signaling is thus a relay of identical pulses, with information encoded in the frequency and pattern of firing rather than in spike magnitude.