The membrane sits at about −70 mV. Na⁺ channels and K⁺ channels are closed; the Na⁺/K⁺ pump and K⁺ leak keep the inside negative.
Think of a resting neuron as a tiny charged battery. The thin membrane keeps the inside of the cell about $70$ millivolts more negative than the outside — that gap is the resting potential, written $-70\ \text{mV}$. The cell spends energy keeping a lot of sodium ($\text{Na}^{+}$) outside and a lot of potassium ($\text{K}^{+}$) inside, like water held behind two separate dams. A nerve signal is simply that voltage flipping positive for an instant and then snapping back.
The membrane is studded with voltage-gated channels — doors that open and close depending on the voltage itself. If a stimulus nudges the voltage up to the threshold of about $-55\ \text{mV}$, the fast $\text{Na}^{+}$ channels fling open and $\text{Na}^{+}$ floods in, driving the inside positive (up to about $+35\ \text{mV}$): this is depolarization. The $\text{Na}^{+}$ channels then inactivate, the slower $\text{K}^{+}$ channels open, and $\text{K}^{+}$ pours out, dragging the voltage back down: repolarization. The whole spike lasts only $1\text{–}2\ \text{ms}$.
The spike is all-or-none: reach threshold and you always get a full-size action potential; fall short and nothing happens. A stronger stimulus does not make a taller spike — it makes the neuron fire more often, so intensity is coded as frequency. After the peak, $\text{K}^{+}$ channels close slowly, so the voltage briefly dips below rest to about $-80\ \text{mV}$ (hyperpolarization). While $\text{Na}^{+}$ channels are inactivated the neuron is refractory — it cannot re-fire — which limits firing rate and forces the signal to travel one way down the axon. The Na⁺/K⁺ pump ($3\ \text{Na}^{+}$ out for $2\ \text{K}^{+}$ in) quietly restores the gradients.
Press Fire! and follow the bright dot climbing the graph as $\text{Na}^{+}$ pours inward, then watch it fall as $\text{K}^{+}$ leaves and dip into the undershoot. Now drag Stimulus strength low and press Step: the voltage rises a little but never reaches $-55\ \text{mV}$, so no spike fires — that is the all-or-none rule in action. Toggle the Na⁺/K⁺ pump on and off to see who restores the gradients, and rotate the membrane to see the channels span it from outside to inside.
| Phase | What happens |
|---|---|
| 1. Resting | Membrane at about $-70\ \text{mV}$. Voltage-gated channels closed; $\text{K}^{+}$ leak and the Na⁺/K⁺ pump hold the inside negative. |
| 2. Threshold | A stimulus depolarizes the membrane to about $-55\ \text{mV}$. If it reaches threshold, the spike will fire; if not, nothing happens. |
| 3. Depolarization | Voltage-gated $\text{Na}^{+}$ channels open; $\text{Na}^{+}$ rushes in and the voltage shoots up to roughly $+35\ \text{mV}$. Sodium entry opens more channels — positive feedback. |
| 4. Repolarization | $\text{Na}^{+}$ channels inactivate and voltage-gated $\text{K}^{+}$ channels open; $\text{K}^{+}$ flows out and the voltage falls back toward rest. |
| 5. Hyperpolarization | $\text{K}^{+}$ channels close slowly, so a little extra $\text{K}^{+}$ leaves and the voltage undershoots to about $-80\ \text{mV}$. |
| 6. Recovery (pump) | $\text{K}^{+}$ channels finish closing and the membrane returns to $-70\ \text{mV}$. The Na⁺/K⁺ pump restores the ion gradients ($3\ \text{Na}^{+}$ out : $2\ \text{K}^{+}$ in). |
At rest the membrane is far more permeable to $\text{K}^{+}$ than to $\text{Na}^{+}$, because many $\text{K}^{+}$ leak channels are open. $\text{K}^{+}$ diffuses outward down its gradient, carrying positive charge out and leaving the inside negative, until the electrical pull inward balances the chemical push outward. The voltage settles near the potassium equilibrium potential, close to $-70\ \text{mV}$. The Na⁺/K⁺ pump does not set the voltage directly; it maintains the concentration gradients that make the whole system work.
$\text{Na}^{+}$ entering at one spot depolarizes the next patch of membrane to threshold, opening its channels, so the action potential regenerates itself down the axon at full strength rather than fading like a passive signal. In myelinated axons the impulse leaps between the bare nodes of Ranvier — saltatory conduction — which is much faster and more energy-efficient. The refractory zone left behind each spike keeps it moving in one direction.
An action potential is a brief, rapid reversal of the voltage across a neuron’s membrane that travels along the axon and carries the nerve signal. At rest the inside of the neuron is about 70 millivolts more negative than the outside. When a stimulus pushes the voltage up to a threshold of about −55 mV, voltage-gated sodium channels snap open, sodium ions rush in, and the inside briefly becomes positive, reaching roughly +30 to +40 mV. Then sodium channels close and voltage-gated potassium channels open, potassium flows out, and the voltage drops back down and even dips slightly below rest before settling. The whole spike lasts only about one to two milliseconds.
Key takeaway: an action potential is a fast, self-propagating swing from negative to positive and back, produced by sodium rushing in and then potassium flowing out.The resting potential comes from unequal ion concentrations plus selective leak channels. The sodium-potassium pump constantly moves three sodium ions out for every two potassium ions it brings in, using ATP, building up sodium outside and potassium inside. At rest the membrane is far more permeable to potassium than sodium because many potassium leak channels are open, so potassium diffuses out down its gradient, carrying positive charge with it and leaving the inside negative. The voltage settles near −70 mV, close to potassium’s equilibrium value, where the outward push from concentration balances the inward pull of the negative interior.
Key takeaway: the resting potential is mainly set by potassium leaking out through open channels, with the pump maintaining the gradients that make this possible.The action potential is all-or-none because once the membrane reaches threshold the spike fires at its full size every time, and if threshold is not reached nothing happens at all. There is no half action potential. A stronger stimulus does not make a bigger spike; it makes the neuron fire more often, so the brain encodes intensity as a higher firing frequency rather than a taller spike. This happens because opening voltage-gated sodium channels is regenerative: a little depolarization opens a few channels, the sodium that enters depolarizes the membrane further, which opens even more channels, in a positive feedback loop that always drives the voltage to the same peak.
Key takeaway: an action potential either fires completely or not at all, and a stronger stimulus raises the firing rate, not the height of each spike.These terms name the phases of the voltage change. Depolarization is when the membrane becomes less negative and then positive, driven by sodium rushing in through open voltage-gated sodium channels; the voltage climbs from −70 toward +35 mV. Repolarization is the return toward negative values, driven by potassium leaving through voltage-gated potassium channels after the sodium channels have closed and inactivated. Hyperpolarization, or the undershoot, is a brief dip below the resting potential to about −80 mV because the slow potassium channels stay open a little too long, letting extra potassium leave before they close.
Key takeaway: depolarization is sodium in and the voltage rising, repolarization is potassium out and the voltage falling, and hyperpolarization is the short overshoot below rest before returning to −70 mV.Both open in response to voltage, but they differ in timing and in how they shut. Voltage-gated sodium channels open very fast at threshold and then automatically inactivate within about a millisecond, plugging themselves with an inactivation gate even though the membrane is still depolarized; this fast inactivation ends the rising phase and helps create the refractory period. Voltage-gated potassium channels open more slowly, stay open while the membrane is depolarized, and close slowly when the voltage falls, which is why potassium keeps leaving a bit too long and causes the undershoot. Sodium channels have two gates, an activation gate and an inactivation gate, while potassium channels effectively have one slower gate.
Key takeaway: sodium channels open fast and self-inactivate to drive the spike up, while potassium channels open slowly and close slowly to bring the voltage back down.The refractory period is a short window right after an action potential when the neuron cannot fire normally again. During the absolute refractory period the sodium channels are inactivated and cannot reopen no matter how strong the stimulus, so no new spike is possible. During the following relative refractory period some sodium channels have reset but the membrane is hyperpolarized, so only an unusually strong stimulus can trigger another spike. This matters for two reasons: it sets an upper limit on how fast a neuron can fire, and it forces the action potential to travel one way down the axon, because the region just behind the spike is still refractory.
Key takeaway: the refractory period is the recovery time set by inactivated sodium channels, and it both limits firing rate and keeps the signal moving forward.An action potential propagates because the local inflow of sodium at one point depolarizes the neighboring patch of membrane to threshold, triggering its channels to open, so the spike regenerates itself step by step along the axon without losing strength. In unmyelinated axons this is continuous and relatively slow. Many axons are wrapped in myelin, a fatty insulating sheath made by glial cells, with small bare gaps called nodes of Ranvier. Because myelin stops ions leaking across the covered regions, the signal jumps from node to node in a fast process called saltatory conduction, greatly increasing speed and saving energy. Loss of myelin, as in multiple sclerosis, slows or blocks conduction.
Key takeaway: the action potential regenerates itself along the membrane, and myelin speeds it up by forcing the signal to leap between the nodes of Ranvier.