An action potential is a rapid, temporary change in a neuron’s electrical voltage that allows it to transmit information over long distances. It occurs when voltage-sensitive ion channels in the cell membrane open and close in a precise sequence, allowing charged particles to move across the membrane. This process produces an electrical impulse that travels along the neuron’s axon and can trigger the release of chemical messengers at a synapse.
Action potentials are essential for communication throughout the nervous system. They help carry sensory information from the skin to the brain, transmit commands from the brain to muscles, and coordinate activity within networks of neurons. Although the signal travels along the cell as a wave of changing electrical conditions, the ions themselves move only relatively short distances across the membrane.
What is an action potential?
Neurons communicate using electrical and chemical signals. An action potential is the electrical signal that travels along the membrane of a neuron, particularly its axon, which is the long projection that carries signals away from the cell body.
Unlike a gradual change in voltage, an action potential is an all-or-none event. Once the membrane reaches a critical voltage called the threshold, a rapid sequence of ion-channel openings generates a stereotyped electrical pulse. If the threshold is not reached, the neuron does not produce a full action potential.
The voltage changes because the inside and outside of the neuron contain different concentrations of electrically charged particles, called ions. Sodium ions carry a positive charge, as do potassium ions, while chloride ions carry a negative charge. These ions are distributed unevenly across the cell membrane.
The membrane acts as a selective barrier. Ion channels allow particular ions to cross it, and the movement of those ions changes the electrical potential between the inside and outside of the cell. During an action potential, this voltage changes rapidly and then returns toward its resting level.
The signal is brief, usually lasting only a few milliseconds in many neurons, but it can travel along an axon that extends a considerable distance. The combination of rapid signaling and reliable propagation allows the nervous system to coordinate activities across the body.
How a neuron maintains its resting electrical potential
Before an action potential can occur, a neuron maintains a voltage difference across its membrane called the resting membrane potential. In many neurons, this potential is approximately −70 millivolts, meaning the inside of the cell is electrically negative relative to the outside. The precise value varies with the type of neuron and its physiological condition.
This voltage arises from the unequal distribution of ions across the membrane and the membrane’s selective permeability to them.
Sodium ions are generally more concentrated outside the neuron, while potassium ions are more concentrated inside. Large negatively charged molecules and proteins also remain inside the cell. Because the membrane at rest is more permeable to potassium than to sodium, potassium ions tend to move outward through open potassium channels. This movement leaves the inside relatively negative.
The resulting electrical force opposes further potassium movement. As positive charges leave the cell, the negative interior attracts them back toward the inside. The resting membrane potential reflects the balance of these electrical and chemical forces, along with the contributions of other ions.
The sodium-potassium pump helps maintain the concentration differences that make this electrical signaling possible. Using energy from ATP, a molecule that supplies energy for cellular processes, the pump moves three sodium ions out of the cell for every two potassium ions it brings in. This active transport maintains the ion gradients over time.
The pump does not directly generate the rapid up-and-down voltage changes of each action potential. Instead, it preserves the conditions needed for repeated signaling. Ion channels produce the rapid electrical changes, while transport mechanisms such as the sodium-potassium pump help restore and maintain the underlying concentration gradients.
How an action potential begins
An action potential usually begins in a neuron’s trigger zone, commonly the axon initial segment near the junction between the cell body and the axon. This region contains many voltage-gated sodium channels, which respond to changes in membrane voltage.
Neurons receive inputs from other neurons through synapses. These inputs can produce small changes in membrane voltage. Excitatory inputs tend to make the inside of the receiving neuron less negative, a change called depolarization. Inhibitory inputs tend to oppose depolarization or make the inside more negative, depending on the channels and conditions involved.
These voltage changes can spread toward the trigger zone and combine. If the combined effect brings the membrane to threshold, enough voltage-gated sodium channels open to initiate an action potential.
Threshold is not a universal fixed voltage. It varies among neurons and can change with the recent activity of the cell and the state of its ion channels. The key event is the opening of enough sodium channels to create a self-amplifying response.
Once sodium enters the cell, the membrane depolarizes further. That additional depolarization opens more voltage-gated sodium channels, allowing still more sodium to enter. This positive feedback produces the rapid rising phase of the action potential.
If the membrane remains below threshold, the sodium-channel activation does not develop into this regenerative event. Small voltage changes can still occur and influence the neuron’s activity, but they do not become full action potentials.
The four main phases of an action potential
An action potential follows a characteristic sequence of electrical changes. The exact voltages and timing depend on the neuron, but the underlying mechanisms are broadly similar in many nerve cells.
1. Depolarization
Once threshold is reached, voltage-gated sodium channels open rapidly. Sodium ions flow into the neuron because both their concentration gradient and the electrical gradient favor inward movement.
As positive charge enters, the inside of the membrane becomes less negative. The voltage can rise from its resting value to a positive level, often reaching approximately +30 to +40 millivolts in a typical neuron.
The inside of the cell is now temporarily positive relative to the outside. This reversal of membrane polarity is a defining feature of the action potential.
The rapid rise depends on the opening of sodium channels and the regenerative feedback between depolarization and further channel activation. It is not caused by the entire inside of the neuron becoming uniformly positive; rather, the voltage difference across a small region of membrane changes.
2. Repolarization
The rising phase does not continue indefinitely. Voltage-gated sodium channels begin to inactivate, meaning they stop conducting sodium even though the membrane remains depolarized. At the same time, voltage-gated potassium channels, which open more slowly, allow potassium ions to flow out of the cell.
The outward movement of positive potassium ions helps make the inside negative again. This return toward the resting voltage is called repolarization.
Sodium-channel inactivation is especially important because it stops the strong inward sodium current that drives the rising phase. Meanwhile, the increased outward potassium current helps reverse the voltage change.
The coordinated timing of these processes makes the action potential a brief pulse rather than a sustained state of depolarization.
3. Hyperpolarization
Potassium channels do not all close immediately when the membrane voltage returns toward its resting level. Some remain open briefly, allowing additional potassium to leave the cell.
As a result, the membrane potential can become more negative than its usual resting value. This phase is called afterhyperpolarization, or simply hyperpolarization.
During this period, the membrane is temporarily farther from threshold in many neurons, making another action potential less likely in response to the same input.
As the potassium channels close and other membrane currents continue, the voltage returns toward its resting level.
4. Return to the resting state
After the action potential, the membrane returns toward its usual resting voltage, and the neuron can respond to further stimulation. Sodium channels recover from inactivation, becoming available to open again when the membrane is sufficiently depolarized.
The ion concentrations do not return to their original values after every individual action potential through the action of the sodium-potassium pump alone. Instead, the pump continuously maintains the concentration gradients, while channels and other transport mechanisms regulate ion movement. The amount of sodium and potassium exchanged during a single action potential is small relative to the total ionic reservoirs.
This distinction matters because the rapid electrical pulse and the slower maintenance of ion concentrations are related but different processes.
How an action potential travels along an axon
An action potential does not move along an axon as a single group of ions traveling from one end to the other. Instead, it propagates as neighboring sections of the membrane generate successive action potentials.
When one section of the axon depolarizes, positive charge spreads locally through the interior of the cell. This current changes the voltage in adjacent sections of the membrane. If a neighboring section reaches threshold, its voltage-gated sodium channels open and a new action potential begins there.
The newly activated section then influences the next section, continuing the process along the axon. In this way, the signal is regenerated as it travels. It does not simply fade away like a passive electrical change would.
The local electrical currents extend beyond the small region where the action potential is occurring, but the full action potential is recreated only where the membrane’s voltage-sensitive channels are activated. This regeneration allows the signal to travel over long distances without progressively losing its amplitude.
The process is normally directed toward the axon terminals because the membrane just behind the advancing signal is temporarily refractory. During the absolute refractory period, many sodium channels remain inactivated, so that section of membrane cannot immediately generate another action potential. During the relative refractory period, another action potential is possible, but it generally requires stronger stimulation.
These refractory periods help ensure reliable propagation and limit how rapidly a neuron can fire repeatedly.
Why some action potentials travel faster than others
The speed of an action potential depends partly on the axon’s diameter and whether the axon is covered by myelin, an insulating material produced by specialized glial cells.
Larger-diameter axons generally conduct signals faster because electrical current encounters less resistance as it spreads along the inside of the cell. However, increasing axon diameter requires more space and biological resources, so it is not the only way the nervous system improves conduction speed.
Myelin provides another solution. It wraps around sections of the axon, reducing the amount of electrical current that leaks across the membrane and making it easier for voltage changes to spread farther along the axon.
In myelinated axons, action potentials are regenerated mainly at gaps in the myelin called nodes of Ranvier. These nodes contain high concentrations of voltage-gated ion channels. The electrical current spreads rapidly beneath the myelin from one node to the next, bringing the next node to threshold.
This process is called saltatory conduction. The term describes the apparent jumping of the signal from node to node, although the underlying current spreads continuously along the axon between them.
Because fewer sections of membrane need to undergo the full sequence of ion-channel opening and closing, saltatory conduction can be substantially faster and more energy-efficient than conduction along an otherwise comparable unmyelinated axon.
Unmyelinated axons also propagate action potentials effectively, but the signal must be regenerated along successive sections of membrane rather than primarily at widely spaced nodes.
How action potentials carry information
An individual action potential is generally an all-or-none event. Once generated, its amplitude does not increase simply because the original stimulus becomes stronger. A stronger stimulus usually changes how frequently a neuron fires, how many neurons become active, or the pattern of activity across a neural population.
For example, a sensory neuron responding to increasing pressure on the skin may produce action potentials at a higher frequency as the pressure increases. The individual action potentials remain broadly similar in size, but their timing and rate provide information about the stimulus.
This principle is known as rate coding, although the nervous system also uses the timing of individual spikes and coordinated activity across multiple neurons to represent information.
A neuron may respond to a weak input with occasional action potentials and to a stronger input with a faster sequence of spikes, up to limits imposed by its refractory periods and other physiological properties. Different neurons can also have different thresholds, firing patterns, and responses to the same input.
Information is therefore not usually encoded by making each action potential proportionally larger. Instead, it is encoded through the activity of neurons over time and across networks.
Action potentials also allow neurons to integrate information from many sources. The small voltage changes produced by incoming signals influence whether the trigger zone reaches threshold. The resulting pattern of action potentials determines how the neuron communicates its output to other cells.
What happens when an action potential reaches a synapse
When an action potential reaches the terminal of a neuron, it can trigger communication with another cell. At a chemical synapse, the arriving electrical signal initiates a sequence of events that converts electrical activity into chemical signaling.
The depolarization of the terminal opens voltage-gated calcium channels. Calcium ions enter the terminal, and the increase in intracellular calcium triggers synaptic vesicles—small membrane-bound sacs containing neurotransmitters—to fuse with the cell membrane.
The vesicles release neurotransmitters into the narrow gap between the two cells, called the synaptic cleft. These chemical messengers cross the gap and bind to receptors on the receiving cell. Depending on the neurotransmitter, receptor, and properties of the receiving membrane, the resulting effect can be excitatory, inhibitory, or modulatory.
At an excitatory synapse, the resulting voltage change may help bring the receiving neuron closer to threshold. At an inhibitory synapse, the effect may reduce the likelihood of an action potential by changing membrane conductance or shifting the membrane voltage in a way that opposes excitation.
The receiving neuron combines these synaptic effects with other incoming signals. If its trigger zone reaches threshold, it generates its own action potential. The signal is therefore transmitted through a sequence of electrical events, with chemical communication connecting many neurons.
Not every action potential produces an identical response at every synapse. Neurotransmitter release can vary, and synaptic strength can change with activity and other physiological conditions. These properties allow neural circuits to adjust how signals influence one another.
Some synapses are electrical rather than chemical. At electrical synapses, specialized channels called gap junctions allow ionic current to pass directly between neighboring cells. This arrangement can transmit voltage changes very rapidly and can help synchronize the activity of connected cells.
Why action potentials are essential to the nervous system
Action potentials allow the nervous system to transmit signals quickly and reliably across distances that small, passive voltage changes could not cover effectively.
When a person touches a hot surface, sensory neurons generate electrical signals that travel toward the spinal cord and brain. Neural circuits process that information, and motor neurons can carry commands to muscles. In a rapid withdrawal reflex, spinal circuits can initiate a response before the brain has fully processed the sensation.
Action potentials also support muscle contraction, including the electrical activation of cardiac muscle that helps coordinate the heartbeat. In the brain, they enable communication among neurons involved in perception, movement, attention, memory, and other functions.
Their importance depends not only on the existence of electrical impulses but also on their timing, frequency, propagation speed, and coordination across networks. Changes in any of these properties can alter how information moves through the nervous system.
The mechanisms that generate action potentials must also remain carefully regulated. Disruptions in ion channels, ion concentrations, or myelin can interfere with electrical signaling. For example, damage to myelin can slow or block conduction in affected axons, while abnormal ion-channel activity can alter the threshold, duration, or frequency of neuronal firing.
An action potential is therefore more than a brief voltage spike. It is a precisely regulated biological process that converts local membrane changes into a traveling electrical signal, allowing neurons to communicate reliably and coordinate the activities of the nervous system.
