Depolarization is the direct trigger for an action potential, but only when it’s strong enough to reach a critical voltage called the threshold. A typical neuron rests at around -70 mV, and the threshold sits near -55 mV. If depolarization pushes the membrane voltage past that point, an action potential fires. If it falls short, nothing happens.
Understanding this relationship means understanding a chain reaction: how a small electrical shift can snowball into a full nerve signal, and why the nervous system has built-in rules that keep this process controlled and predictable.
How Depolarization Triggers the Threshold
Neurons maintain a negative internal charge at rest because of the way ions are distributed across their membranes. Depolarization is any event that makes the inside of the cell less negative. This can come from a neighboring neuron releasing a chemical signal, a sensory receptor responding to touch or heat, or an electrical stimulus applied in a lab.
The key players are sodium channels embedded in the neuron’s membrane. These channels are normally closed, but they’re sensitive to voltage. When the membrane depolarizes enough to reach threshold, these channels snap open and let positively charged sodium ions rush into the cell. That influx of sodium makes the inside of the cell even more positive, which opens even more sodium channels, which lets in even more sodium. This positive feedback loop is what creates the rapid, dramatic voltage spike of an action potential, driving the membrane potential from around -55 mV all the way up toward +30 or +40 mV in roughly one millisecond.
The critical insight is that the sodium channels don’t just respond to depolarization passively. They amplify it. Once enough of them open, the process becomes self-sustaining and unstoppable. That’s why there’s a sharp dividing line between “not enough depolarization” and “full action potential.”
Why Small Depolarizations Don’t Count
Not every depolarization produces an action potential. When a neuron receives a weak signal, its membrane voltage might shift from -70 mV to -65 mV. That’s a depolarization, but it’s below threshold. These sub-threshold shifts are called graded potentials, and they behave very differently from action potentials.
Graded potentials fade as they travel along the membrane. Sodium ions leak back out, the voltage drops, and the signal weakens over distance. If a graded potential isn’t strong enough when it reaches the part of the neuron where action potentials are initiated (a region called the axon hillock), no action potential occurs. The signal simply dies out. This is why graded potentials can’t carry information over long distances the way action potentials can.
The All-or-None Rule
Action potentials follow a strict binary: they either fire completely or don’t fire at all. There’s no such thing as a “half” action potential or a “strong” one. Once threshold is reached, every action potential in a given neuron has the same size and shape. A stronger stimulus doesn’t create a bigger spike.
So how does the nervous system encode intensity? Not through bigger signals, but through faster ones. A stronger stimulus causes a neuron to fire more action potentials per second, and it recruits more neurons to fire simultaneously. Your brain interprets a light touch versus a hard press based on firing frequency and how many neurons are involved, not on the size of individual signals.
How Weak Signals Add Up
A single incoming signal often produces a graded potential of only about 1 mV, far too small to reach threshold on its own. The nervous system solves this through summation, the process of stacking multiple small signals together.
Spatial summation happens when several neurons send signals to the same target at the same time. Each one contributes a small depolarization, and if enough arrive simultaneously, their combined effect pushes the membrane past threshold. Temporal summation happens when a single neuron fires repeatedly in quick succession. Each signal arrives before the previous one has fully faded, so the depolarizations pile on top of each other. Both mechanisms allow the nervous system to fine-tune which neurons fire and when, giving the brain precise control over its responses.
What Happens After the Spike
The action potential doesn’t last long. About one millisecond after the sodium channels open, they automatically inactivate, slamming shut regardless of the membrane voltage. At the same time, a separate set of voltage-sensitive channels opens to let potassium ions flow out of the cell. Since potassium carries a positive charge, its exit pulls the membrane voltage back down. This is repolarization.
The potassium channels are slightly slow to close, so the membrane voltage temporarily dips below its normal resting level, a brief phase called hyperpolarization. The cell then gradually returns to its resting state as ion pumps restore the original balance of sodium outside and potassium inside.
The Refractory Period
Immediately after an action potential, the neuron enters a brief window where it can’t fire again. This is called the absolute refractory period, lasting about 0.4 milliseconds. During this time, the sodium channels are physically inactivated. No amount of stimulation will produce another action potential. This puts a ceiling on how fast a neuron can fire, roughly 2,500 times per second at maximum.
Following the absolute refractory period is the relative refractory period, which overlaps with the hyperpolarization phase. Here, firing is possible but harder. Because the membrane is temporarily more negative than usual and potassium channels are still open, a stronger-than-normal stimulus is needed to reach threshold. This period gradually fades as the membrane returns to rest.
The refractory period also serves an important directional purpose. Because the section of membrane that just fired can’t immediately fire again, the action potential can only move forward along the nerve fiber. It can’t loop back on itself.
Depolarization Without Sodium Channels
In most neurons, voltage-sensitive sodium channels are the critical link between depolarization and action potential. But the broader principle is the same in other excitable cells. Heart muscle cells, for example, also use sodium channels for their initial rapid depolarization, though their action potentials last much longer because calcium channels play an additional role in sustaining the signal. Pacemaker cells in the heart use a slightly different mechanism to generate their rhythmic depolarizations, but the core concept holds: depolarization past a threshold voltage triggers a self-reinforcing electrical event.
The relationship between depolarization and action potentials is causal but conditional. Depolarization is necessary, it is the only natural way to open the voltage-sensitive channels that produce an action potential. But it’s only sufficient when it reaches threshold. Below that line, you get a graded potential that fades. Above it, you get the full regenerative spike that carries signals from one end of a nerve fiber to the other.