A neuron’s electrical signal is not electricity in the same sense as current flowing through a copper wire. It is a carefully controlled movement of charged particles across the neuron’s membrane. The result is a rapid, self-propagating change in membrane voltage called an action potential.
Understanding this matters in epilepsy because seizures emerge from networks of neurons whose electrical behaviour becomes excessively synchronised, abnormally excitable or both. The action potential is therefore one of the basic building blocks of seizure physiology — but it is not itself a seizure.
The membrane is the starting point
Every neuron is enclosed by a lipid membrane that separates the fluid inside the cell from the fluid outside it. Ions such as sodium (Na+), potassium (K+), chloride (Cl−) and calcium (Ca2+) are distributed unequally across that membrane. Because ions carry electrical charge, this unequal distribution creates an electrical potential across the membrane.
At rest, the inside of a typical neuron is negative relative to the outside. The exact value varies by cell type, but a commonly cited resting membrane potential is around −70 millivolts. Potassium permeability has a major influence on this resting state because the membrane is relatively permeable to K+ through leak channels.
The sodium-potassium pump does not fire the action potential
The sodium-potassium ATPase is essential because it maintains the long-term sodium and potassium concentration gradients that electrical signalling depends on. It uses energy from ATP to move sodium out of the cell and potassium into it.
A common simplification is that the pump directly creates each nerve impulse. It does not. The millisecond-by-millisecond shape of an action potential is produced mainly by ions flowing through voltage-gated channels. The pump restores and preserves the gradients that make repeated signalling possible.
From small voltage change to threshold
Neurons are constantly receiving synaptic inputs. Some make the membrane potential less negative, or depolarise it; others make firing less likely. These inputs are integrated across the cell, especially near the axon initial segment, where there is a high density of voltage-gated sodium channels.
If depolarisation reaches a critical threshold, enough sodium channels open to start a regenerative process. Sodium enters the neuron down its electrochemical gradient, making the inside rapidly more positive. That additional depolarisation opens still more sodium channels. This positive-feedback loop produces the steep rising phase of the action potential.
Why an action potential is all-or-none
Once threshold is crossed, the regenerative opening of voltage-gated sodium channels drives the membrane through a stereotyped action potential. A stronger stimulus does not usually produce a proportionally taller action potential. Instead, information is often encoded by how frequently neurons fire and by which neurons fire together.
This all-or-none behaviour is why threshold matters. Subthreshold inputs can change membrane voltage without producing a full action potential; suprathreshold depolarisation triggers the regenerative response.
Repolarisation: how the spike ends
The rising phase cannot continue indefinitely. Voltage-gated sodium channels rapidly inactivate, while voltage-gated potassium channels open more slowly. Potassium then leaves the cell, moving the membrane potential back towards negative values. This is repolarisation.
Because some potassium channels remain open briefly, the membrane may become more negative than its usual resting level. This is often called after-hyperpolarisation.
The refractory period
Immediately after an action potential, many sodium channels are in an inactivated state and cannot reopen straight away. This produces an absolute refractory period. A later relative refractory period follows, during which another action potential is possible but requires stronger depolarisation than usual.
Refractory periods help limit firing frequency and make ordinary action potentials travel predominantly forward along the axon rather than repeatedly re-exciting the membrane behind them.
How the signal travels down the axon
An action potential at one section of axon creates local current that depolarises the neighbouring membrane. If that neighbouring membrane reaches threshold, a new action potential is generated there. In this way the signal is regenerated along the axon rather than fading like a passive voltage change.
In myelinated axons, voltage-gated channels are concentrated at gaps in the myelin called nodes of Ranvier. The signal effectively moves from node to node, a process called saltatory conduction, which greatly increases conduction speed and reduces energy demand.
What happens at the synapse
When an action potential reaches a presynaptic terminal, it opens voltage-gated calcium channels. Calcium entering the terminal triggers neurotransmitter-containing vesicles to fuse with the presynaptic membrane and release their contents into the synaptic cleft.
The neurotransmitter then binds receptors on the next cell. Depending on the receptor and ion channels involved, the postsynaptic effect may increase or decrease the probability that the next neuron reaches threshold. This is where action potentials connect to the wider balance of excitation and inhibition.
Ion channels are not all the same
Neurons contain many families of ion channels. Some respond to voltage, some to neurotransmitters or other ligands, and others to intracellular signals, mechanical forces or temperature. Even within one family, different channel subtypes can open at different voltages, activate or inactivate at different speeds, and be distributed in different parts of the neuron.
This diversity is one reason different neurons can have very different firing patterns despite using the same basic ions. It is also one reason mutations affecting ion-channel genes can produce very different epilepsy phenotypes.
Where epilepsy enters the picture
Epilepsy can involve altered neuronal excitability at several levels. Genetic variants may change ion-channel function. Structural lesions can reorganise local circuits. Inflammation, gliosis, altered receptor expression, neurotransmitter imbalance and changes in network connectivity can all affect how easily neurons and networks fire together.
That means there is no single “epilepsy voltage” or one abnormal channel found in every person with epilepsy. The same final event — a seizure — can arise from many different biological routes.
Action potentials are not the same as EEG waves
An EEG does not record individual action potentials from single neurons at the scalp. Scalp EEG mainly reflects summed postsynaptic electrical activity from large populations of synchronously active cortical neurons. Individual action potentials are too small and spatially restricted to be detected directly in this way.
This distinction matters because seizure activity is a network phenomenon. A neuron firing an action potential is normal physiology; millions of neurons participating in abnormal synchronised activity is something very different.
What experiments established this model?
The modern understanding of the action potential was built from electrophysiology, especially voltage-clamp experiments showing that sodium and potassium conductances change with membrane voltage and time. Later patch-clamp techniques allowed currents through single ion channels to be measured directly, confirming that voltage-sensitive, ion-selective channels underlie the electrical behaviour predicted by earlier models.
What this page does — and does not — explain
This page explains the electrical signal of an individual neuron. It does not explain how excitation and inhibition are balanced across circuits, how seizures spread through networks, or how an epileptic brain becomes persistently seizure-prone. Those are separate questions covered elsewhere in the Science & Discovery section.
Sources
NCBI Bookshelf — The Ionic Basis of Action Potentials
NCBI Bookshelf — Ion Channels Underlying Action Potentials
NCBI Bookshelf — Channels and Transporters
NCBI Bookshelf — Ion Channels and the Electrical Properties of Membranes
Evidence checked: September 2026.