Resting Membrane Potential and Action Potential

The resting membrane potential. A resting neuron is electrically polarized: the inside is about −70 millivolts (mV) relative to the outside. This is set up by two things introduced earlier: the sodium–potassium pump (which keeps sodium (Na⁺) high outside and potassium (K⁺) high inside) and the membrane's greater leakiness to K⁺. The result is a charged, "ready" membrane — like a loaded spring waiting to fire.

The action potential. When a stimulus depolarizes the membrane to a critical threshold, voltage-gated channels open and a rapid, all-or-nothing electrical event — the action potential — sweeps down the axon. Its phases:

1. Resting state: membrane at −70 mV; channels closed.
2. Depolarization: at threshold, sodium channels open and Na⁺ rushes in, making the inside rapidly less negative and then positive (a spike toward about +30 mV).
3. Repolarization: sodium channels close and potassium channels open, so K⁺ flows out, returning the inside toward negative.
4. Return to rest: a brief overshoot (hyperpolarization) settles back to −70 mV; the sodium–potassium pump restores the original ion distribution.

Two key properties: the action potential is all-or-none (it either reaches threshold and fires fully, or it doesn't), and a brief refractory period afterward prevents the signal from running backward and sets a maximum firing rate.

Propagation. An action potential is self-propagating: the depolarization at one spot triggers the next patch of membrane to reach threshold, and so on down the axon — like a row of dominoes or a lit fuse. This one-way wave carries the signal from the cell body to the axon terminals.

Myelin and saltatory conduction. In myelinated axons, the insulating myelin forces the action potential to regenerate only at the gaps between myelin segments (nodes). The impulse therefore appears to jump from gap to gap — saltatory conduction (from Latin saltare, "to leap") — which is far faster and more energy-efficient than continuous conduction along an unmyelinated axon. This is why myelin loss (as in multiple sclerosis) slows signals so dramatically.

How it works

The signal in sequence:

Rest (−70 mV) → stimulus reaches threshold
   → Na⁺ channels open → Na⁺ in → DEPOLARIZATION (spike to ~+30 mV)
   → Na⁺ channels close, K⁺ channels open → K⁺ out → REPOLARIZATION
   → brief hyperpolarization → Na⁺/K⁺ pump restores rest
Signal propagates down the axon (jumping node to node if myelinated)

Comparisons

Common confusions

• Depolarization vs repolarization. Depolarization = becoming less negative (Na⁺ in); repolarization = returning to negative (K⁺ out).
• Resting potential is negative inside (~−70 mV), maintained by the Na⁺/K⁺ pump.
• All-or-none. Stronger stimuli don't make a bigger action potential; they make them fire more often.
• Saltatory conduction "jumps" at nodes — myelin doesn't slow the signal; it speeds it.

Memory aids

• "Depolarize = Na⁺ Dashes in; Repolarize = K⁺ Kicks out."
• Resting = "−70, negative and ready."
• Saltatory = "salt/leap — the signal jumps."

Quick review

• A resting neuron sits at about −70 mV (inside negative), maintained by the Na⁺/K⁺ pump.
• An action potential: reaching threshold opens Na⁺ channels (depolarization, Na⁺ in), then K⁺ channels (repolarization, K⁺ out); it is all-or-none with a refractory period.
• The impulse self-propagates one-way down the axon.
• Myelin enables saltatory conduction (the signal jumps node to node), greatly increasing speed; anesthetics and electrolyte imbalances act on these ion movements.