How a Nerve Signal Travels
A thought, a heartbeat, a flinch away from a hot stove — every one of them is an electrical pulse racing down a nerve. That pulse is the action potential: a wave of voltage that flips the axon membrane from −70 mV to +40 mV and back, then leaps node to node down the wire. Watch the tiny Na⁺/K⁺ pump keep the resting battery charged, then drag the Stimulus strength slider to discover the −55 mV threshold: too weak and nothing happens; strong enough and the axon fires a full, all-or-nothing spike — and a stronger stimulus fires faster, not bigger.
What's happening
The Science in Plain Language
1. Resting potential (−70 mV). A nerve at rest is like a charged battery. A tiny protein pump called the Na⁺/K⁺ pump runs constantly, burning one molecule of ATP to push three sodium ions (Na⁺) out of the axon and pull two potassium ions (K⁺) in. Because it ejects more positive charge than it imports, and because the membrane leaks K⁺ back out, the inside settles at about −70 millivolts relative to the outside. Nothing is “happening,” but the cell is loaded and ready — you can watch the pump ticking in the diagram.
2. Threshold & all-or-nothing. When a stimulus nudges the membrane up to about −55 mV (the threshold), voltage-gated channels snap open and the cell fires. Crucially, an action potential is all-or-nothing: a bigger stimulus does not make a bigger spike. Slide Stimulus strength below +15 mV and the membrane bulges a little but never fires (a subthreshold graded potential); slide it above +15 mV and a full-size spike erupts every time. Strength is coded by how often the axon fires, not how big each spike is — turn on Sustained stimulus and watch the firing-rate readout climb as you raise the stimulus.
3. Depolarization (Na⁺ rushes IN). At threshold, sodium channels fling open and Na⁺ floods into the axon, chasing both its concentration gradient and the negative charge inside. In under a millisecond the inside flips from negative to positive (about +40 mV). This is the rising edge of the spike you see on the oscilloscope.
4. Repolarization (K⁺ flows OUT). The sodium channels quickly slam shut, and slower potassium channels open. K⁺ pours out of the axon, carrying positive charge with it, and the membrane potential plunges back down toward −70 mV — often briefly overshooting to about −80 mV (a short hyperpolarization). The Na⁺/K⁺ pump then quietly restores the original ion balance.
5. The refractory period (why signals go one way). Right after firing, the sodium channels are temporarily locked and cannot reopen — this is the refractory period. Because the patch of membrane just behind the impulse is briefly “unfireable,” the wave can only move forward, never backward. That's what makes a nerve signal travel in a single, reliable direction. The refractory period also caps the maximum firing rate, which is why frequency coding tops out around 100–500 spikes per second even for the strongest stimulus.
6. Saltatory conduction (myelin makes it jump). Long axons are wrapped in fatty myelin sheath with bare gaps called nodes of Ranvier. Myelin insulates the axon so the electrical charge zips passively under each sheath and the action potential only regenerates at the exposed nodes — so the impulse appears to jump node to node (Latin saltare, “to leap”). This makes signals dramatically faster (up to ~120 m/s) while using far less energy. When myelin is destroyed — as in multiple sclerosis — the jumps break down, signals slow or fail, and the result is weakness, numbness, and vision or coordination problems.
7. The synapse (handoff to the next cell). When the impulse reaches the axon terminal, its voltage swing triggers calcium entry, and tiny sacs (vesicles) release chemical messengers called neurotransmitters into the microscopic synaptic gap. They drift across and bind receptors on the next cell, either nudging it toward its own threshold or telling it to stay quiet. One electrical pulse becomes a chemical message — and the relay continues, cell to cell, across your entire nervous system.