Overview
Nerve and muscle cells are excitable: they can store electrical charge across their membranes and release it in a controlled burst to send signals. That stored charge is the membrane potential, and the traveling burst is the action potential, the nerve impulse. This lesson explains how a neuron builds its charge at rest, fires an impulse, and passes the message to the next cell.
The Resting Membrane Potential
A resting neuron is electrically polarized: the inside is negative relative to the outside, typically about negative 70 millivolts. Two features create this.
First, ions are unevenly distributed. Sodium (Na+) is concentrated outside the cell and potassium (K+) inside, while large negatively charged proteins are trapped inside. Second, the membrane is selectively permeable: at rest it is far more permeable to potassium than to sodium, so potassium leaks outward and leaves the interior negative.
These gradients would run down without maintenance. The sodium-potassium pump prevents that, actively pumping three sodium ions out for every two potassium ions in, using ATP. It restores what leaks and keeps the gradients ready to power an impulse.
Reaching Threshold
A stimulus that makes the inside less negative causes depolarization. Small stimuli produce small local changes that fade. But if depolarization reaches threshold, near negative 55 millivolts, it triggers a full action potential. Below threshold, nothing propagates; at or above it, the impulse fires completely. This is the all-or-none principle: the action potential does not grow larger with a stronger stimulus. Instead, the nervous system codes stimulus intensity as the frequency of impulses.
The Action Potential
Once threshold is crossed, a rapid, stereotyped sequence unfolds.
| Phase | Ion movement | Effect on voltage |
|---|---|---|
| Depolarization | Voltage-gated Na+ channels open; sodium rushes in | Rises toward and past 0 mV (peak near +30 mV) |
| Repolarization | Na+ channels inactivate; voltage-gated K+ channels open; potassium exits | Falls back toward negative |
| Hyperpolarization | K+ channels close slowly; slight overshoot below rest | Briefly more negative than resting |
| Return to rest | Pump and leak channels restore balance | Back to about negative 70 mV |
During and just after the spike, the neuron passes through a refractory period when it cannot easily fire again. This ensures impulses travel in one direction, down the axon, and limits how rapidly they can repeat.
Conduction Along the Axon
An action potential at one point depolarizes the neighboring membrane to threshold, regenerating the impulse further along. On bare (unmyelinated) axons this happens continuously and is relatively slow.
Many axons are wrapped in myelin, a fatty insulating sheath with periodic gaps called nodes of Ranvier. Voltage-gated channels cluster at the nodes, so the action potential regenerates only there and effectively jumps from node to node. This is saltatory conduction, and it makes myelinated fibers dramatically faster and more energy efficient than unmyelinated ones.
Synaptic Transmission
Where a neuron meets its target lies a synapse, usually with a narrow gap between the cells. Most synapses are chemical and work in steps:
- The action potential reaches the axon terminal and depolarizes it.
- Voltage-gated calcium channels open, and calcium enters the terminal.
- Calcium triggers vesicles to fuse with the membrane and release neurotransmitter into the gap.
- Neurotransmitter diffuses across and binds receptors on the target cell.
- Binding opens channels there, either depolarizing the target (excitatory) or making it more negative (inhibitory).
The signal is then terminated as neurotransmitter is broken down, taken back up, or diffuses away, readying the synapse for the next impulse.
Clinical Relevance
Membrane physiology underlies much of clinical medicine. Multiple sclerosis destroys myelin, so saltatory conduction fails and impulses slow or stall, producing weakness, numbness, and visual loss. Local anesthetics such as lidocaine block voltage-gated sodium channels, preventing depolarization from reaching threshold so pain impulses cannot form. Abnormal blood potassium shifts the resting potential and can make the heart dangerously unexcitable or overexcitable, which is why potassium is watched closely in emergency and nursing care. And because ion pumps require ATP, loss of oxygen or fuel to a tissue quickly collapses these gradients, one reason nerve and cardiac cells are so vulnerable to ischemia.