Action Potential in Neurons Explained

What Is an Action Potential?

An action potential is an electrical signal that travels along a neuron's axon. It's how your brain and nervous system communicate. Without it, nothing works — no thought, no reflex, no sensation.

The signal is a brief reversal of electrical charge across the neuron membrane. Sodium ions rush in, then potassium ions rush out. This creates a wave of voltage change that propagates from the cell body down to the axon terminal.

It's not like a wire carrying electricity. It's a self-propagating chain reaction that relies on ion gradients and voltage-sensitive proteins.

The Resting Membrane Potential

Before any signal happens, the neuron sits at rest. The inside of the cell is negatively charged relative to the outside — typically around -70 millivolts.

This charge difference exists because:

The pump uses ATP. It fights the natural flow of ions. Without it, everything would equalize and neurons would go silent.

The Phases of an Action Potential

Depolarization

Something stimulates the neuron — a touch, a neurotransmitter, another action potential. If the stimulus is strong enough to push the membrane past threshold (around -55 mV), voltage-gated sodium channels open.

Sodium floods into the cell. The inside becomes less negative, then positive. Voltage climbs rapidly from -70 mV to about +30 mV.

This is depolarization. The membrane voltage reverses.

Repolarization

At the peak of depolarization, sodium channels inactivate. They don't just close — they enter an inactivated state and won't open again immediately.

Voltage-gated potassium channels now open. Potassium rushes out of the cell, following its concentration gradient. The inside becomes negative again.

Voltage drops back toward resting levels. This is repolarization.

Hyperpolarization

Potassium channels stay open longer than necessary. More potassium leaves than at rest. The membrane voltage dips below -70 mV — it hyperpolarizes.

This is why you see a brief undershoot on a graph of an action potential. The cell is temporarily harder to stimulate during this phase.

Returning to Rest

The sodium-potassium pump restores ion gradients over milliseconds. The membrane settles back at -70 mV, ready for the next signal.

Voltage-Gated Ion Channels

These proteins are the machinery behind everything. They're embedded in the axon membrane and open or close based on membrane voltage.

Sodium Channels

Have two gates: an activation gate (opens on depolarization) and an inactivation gate (closes shortly after opening). The inactivation is why you can't fire another action potential immediately — sodium can't get in.

Potassium Channels

Open more slowly than sodium channels and stay open longer. This timing is what causes repolarization and hyperpolarization.

The difference in opening speed between sodium and potassium channels is what creates the characteristic spike shape of an action potential.

The All-or-None Principle

An action potential either happens completely or it doesn't happen at all. There's no such thing as a half-strength signal.

If the stimulus pushes the membrane past threshold, the response is always the same magnitude. If it stays below threshold, nothing fires.

This doesn't mean the signal can't vary in meaning. Frequency matters. A neuron firing 10 times per second vs 100 times per second carries different information.

Refractory Periods

After an action potential fires, there's a period where another one can't be triggered — or can't be triggered as easily.

Absolute Refractory Period

Sodium channels are inactivated. No amount of stimulation will trigger another action potential. This lasts about 1 millisecond and limits how fast a neuron can fire.

Relative Refractory Period

Some potassium channels are still open. A stronger-than-normal stimulus can trigger another action potential, but threshold is higher. The cell is harder to excite.

Propagation Along the Axon

The action potential doesn't jump — it travels. When sodium enters at one segment, it depolarizes the adjacent segment. That opens sodium channels there, and the cycle repeats.

The signal moves in one direction because the previous segment is in refractory period. It can't fire backward.

Myelination and Saltatory Conduction

Some axons are wrapped in myelin — fatty insulation produced by oligodendrocytes in the CNS and Schwann cells in the PNS.

Myelin prevents current leak. The action potential hops between Nodes of Ranvier — gaps in the myelin where sodium channels are concentrated.

This is saltatory conduction. It's faster and uses less energy than continuous propagation. Your motor neurons need this speed for movement. Slower conduction means slower reactions.

Action Potential vs Graded Potential

These are not the same thing. Know the difference.

Feature Action Potential Graded Potential
Location Axon hillock and axon Dendrites and cell body
Signal type All-or-none Graded (varies with stimulus)
Amplitude Constant (~100 mV) Variable (few mV)
Duration 1-2 milliseconds Longer, variable
Decay Does not decay Decays with distance
Can initiate AP? Yes Only if reaches threshold

Graded potentials integrate incoming information. If they sum and reach threshold at the axon hillock, an action potential fires.

Why This Matters

Action potentials are the foundation of everything the nervous system does. When they fail, the consequences are immediate and severe.

Local anesthetics like lidocaine block voltage-gated sodium channels. The neuron can't fire. You don't feel pain.

Some toxins target ion channels. Tetrodotoxin from pufferfish blocks sodium channels. Nerve agents affect potassium channels. These aren't academic concerns — they're real-world mechanisms of harm.

Conditions like multiple sclerosis involve degradation of myelin. The result is slowed or blocked signal conduction. Symptoms depend on which pathways are affected.

Key Ion Channel Comparison

Property Voltage-Gated Na+ Voltage-Gated K+
Opens at -55 mV (earlier) -40 mV (later)
Opening speed Fast Slower
Closing behavior Inactivates quickly Closes slowly
Role in depolarization Causes it Minimal
Role in repolarization Stops depolarization Drives repolarization
Blocked by Tetrodotoxin, lidocaine Tetraethylammonium

How Action Potentials Are Measured

The classic method is a patch clamp. A glass micropipette forms a tight seal with the membrane. You can measure the tiny currents flowing through individual ion channels.

Voltage clamp keeps the membrane voltage constant and measures the current needed to hold it there. You see the sodium current first, then the potassium current.

Current clamp does the opposite — it injects current and measures the voltage change. This is how you see the actual action potential waveform.

Modern imaging uses voltage-sensitive dyes or genetically encoded indicators. You can watch populations of neurons fire in real time. The trade-off is lower temporal resolution than electrophysiology.

Getting Started: How to Think About Action Potentials

Forget memorizing phases in order. Focus on the mechanism:

  1. Ion gradients exist because of the sodium-potassium pump. This is the battery.
  2. Sodium channels open when the membrane depolarizes past threshold. This is the trigger.
  3. Sodium rushes in because it's driven by both concentration gradient and electrical gradient. The inside becomes positive.
  4. Potassium channels open with a slight delay. Potassium leaves. The inside becomes negative again.
  5. The pump restores gradients. The cycle resets.

The waveform is a consequence of channel kinetics — when each channel type opens and closes. The shape isn't arbitrary. It's determined by the properties of the proteins.

If you want to understand action potentials deeply, study the Hodgkin-Huxley model. Alan Hodgkin and Andrew Huxley worked out the mathematics in the 1950s using squid giant axons. They won the Nobel Prize. The model still holds up.