An action potential is a rapid electrical signal that travels along a nerve cell, carrying information from one part of your body to another. It works like a brief voltage spike: the inside of the cell swings from about -70 millivolts (its resting state) up to +30 millivolts and back again, all within roughly one millisecond. This 100-millivolt swing is the basic unit of communication in your nervous system, responsible for everything from feeling a hot stove to deciding to move your hand away.
How a Nerve Cell Stays Ready to Fire
Before an action potential happens, a nerve cell sits at what’s called its resting membrane potential, typically around -70 mV. That negative number means the inside of the cell is electrically negative compared to the outside. The cell maintains this charge difference by keeping more potassium ions inside and more sodium ions outside, using a molecular pump that runs constantly. Think of it as a loaded spring: the uneven distribution of charged particles stores energy the cell can release on demand.
The resting potential isn’t identical across all cells. Depending on the type of neuron, it can range from -30 mV to -90 mV, but -70 mV is the most commonly cited value for a typical nerve cell.
What Triggers an Action Potential
An action potential fires when a stimulus pushes the cell’s voltage past a critical point called the threshold. In most neurons, this threshold sits somewhere around -55 mV, though measurements at the cell body can range from about -52 mV to -42 mV depending on the neuron. That means the cell needs to be pushed only about 15 millivolts from its resting state to set off the full electrical event.
This is where the “all-or-none” principle comes in. If the stimulus is too weak to reach threshold, nothing happens. But once threshold is crossed, the action potential fires at full strength every time. You can’t get a half-sized or double-sized action potential. Every one peaks at the same +30 mV. The nervous system encodes intensity not by making bigger signals, but by firing more of them per second.
The Four Stages of an Action Potential
Once threshold is reached, the action potential unfolds in a predictable sequence driven by two types of channels in the cell membrane: sodium channels and potassium channels. Both open in response to voltage changes, but they operate on different timelines, and that timing difference creates the signal’s characteristic shape.
Depolarization
Sodium channels open first. Sodium ions rush into the cell, making the inside rapidly more positive. This is a self-reinforcing process: as more sodium enters and the voltage rises, even more sodium channels open, which drives the voltage higher still. This positive feedback loop sends the membrane potential shooting from -55 mV up to +30 mV in a fraction of a millisecond.
Repolarization
Two things happen almost simultaneously to reverse the surge. The sodium channels inactivate, snapping shut even though the voltage is still high. At the same time, potassium channels finally open. These channels are slower to respond to the initial voltage change, so they’re just now catching up. Potassium ions flow out of the cell, carrying positive charge with them and dragging the voltage back down toward -70 mV.
Hyperpolarization
The potassium channels don’t close the instant the voltage hits -70 mV. They stay open a beat too long, so the voltage overshoots, dipping slightly below the resting level. During this brief undershoot, the cell is actually more negative inside than usual. Once the potassium channels close, the resting pumps restore the membrane to its normal -70 mV baseline.
Return to Rest
The molecular pump that maintains the sodium-potassium balance works continuously to reset the ion concentrations. In practice, a single action potential moves so few ions relative to the total supply that the cell can fire thousands of times before the pump would need to fully “catch up.” The cell is effectively ready to fire again almost immediately, with one important caveat: the refractory period.
Why Neurons Need a Cooldown Period
Right after an action potential, the sodium channels aren’t just closed. They’re locked in an inactivated state, physically unable to reopen regardless of how strong a stimulus arrives. This is the absolute refractory period, lasting roughly 1 to 2 milliseconds. During this window, the neuron cannot fire another action potential no matter what.
Following that is the relative refractory period, lasting another 2 to 5 milliseconds. During this phase, the neuron can fire again, but only if it receives a stronger-than-normal stimulus, because the lingering potassium outflow is still pulling the voltage below resting level. Together, these cooldown periods serve two purposes: they cap the neuron’s maximum firing rate at a few hundred signals per second, and they ensure the signal travels in one direction, since the section of membrane behind the signal is temporarily unable to fire.
How the Signal Travels Along the Nerve
An action potential doesn’t just happen in one spot. It propagates down the length of the nerve fiber like a wave. The voltage spike at one point opens sodium channels in the adjacent stretch of membrane, triggering a new action potential there, which triggers the next segment, and so on. Because each section enters its refractory period immediately after firing, the wave can only move forward.
Speed varies enormously depending on the nerve fiber. Thin, bare nerve fibers conduct signals at roughly 0.5 to 10 meters per second. Many important nerves, though, are wrapped in myelin, a fatty insulating sheath with small gaps spaced along the fiber. In myelinated nerves, the electrical signal jumps from gap to gap rather than traveling through every segment of membrane. This jumping conduction pushes speeds up to 150 meters per second, fast enough that a signal from your toe reaches your spinal cord in about a hundredth of a second.
What Happens When the Signal Reaches Its Destination
When an action potential arrives at the end of a nerve fiber, it needs to pass its message to the next cell, whether that’s another neuron, a muscle fiber, or a gland. The electrical signal can’t jump across the tiny gap (synapse) between cells, so the nerve terminal converts it into a chemical signal.
The arriving action potential opens calcium channels at the nerve ending. Calcium ions flood in and activate sensor proteins that physically pull open tiny packets (vesicles) filled with chemical messengers called neurotransmitters. This whole process, from calcium entry to neurotransmitter release, takes just a few hundred microseconds. The released neurotransmitters cross the gap and bind to receptors on the next cell, potentially triggering a new action potential there and continuing the chain of communication.
Action Potentials in the Heart
Nerve cells aren’t the only cells that use action potentials. Heart muscle cells fire them too, but with a dramatically different profile. A neuronal action potential lasts about 1 millisecond. A cardiac action potential lasts 200 to 400 milliseconds, roughly 200 to 400 times longer.
The difference comes from calcium. In heart cells, calcium ions flow in during the middle of the action potential and create a sustained “plateau phase” that keeps the cell electrically active for a prolonged period. This extended signal is what coordinates the long, powerful contraction your heart needs to pump blood effectively. It also gives the heart muscle time to fully relax before the next beat, preventing the kind of rapid re-firing that could cause dangerous rhythm problems.
How Electrolyte Imbalances Disrupt the Process
Because action potentials depend entirely on the movement of charged particles across cell membranes, shifts in your body’s electrolyte levels can have serious effects. Potassium imbalances are particularly impactful.
When potassium levels in the blood rise too high (hyperkalemia), the resting voltage of cells becomes less negative, essentially moving closer to threshold. At first this can make cells easier to excite, but at higher levels it actually inactivates sodium channels, slowing signal conduction and eventually making cells unable to fire at all. In the heart, this can cause dangerous conduction blocks and irregular rhythms.
Low potassium (hypokalemia) has the opposite starting point: the resting voltage becomes more negative than normal, making cells harder to excite. But the downstream effects are equally dangerous. The action potential takes longer to complete, and the extended duration lets excess calcium flow into heart cells. This combination creates conditions ripe for abnormal heartbeats, including rhythms that can degenerate into cardiac arrest. It’s one reason that potassium levels are among the most closely monitored blood values in hospital settings.