Physiology chapters

The nerve action potential

The phases of the action potential and the ion channels behind each, threshold and the all-or-none law, refractory periods, how fast impulses travel, and how potassium and calcium changes alter excitability.

UHS PGET syllabus: Excitable tissue: nerve and muscle (2 MCQs), Action potential: different phases; threshold stimulus; properties; refractory periods; conduction velocity; effect of electrolyte disturbancesUpdated October 2026
In 30 seconds
  • An action potential is a brief reversal of membrane voltage: Na+ rushes in (depolarisation), then K+ flows out (repolarisation).
  • It obeys the all-or-none law: once threshold is reached it fires fully; otherwise not at all.
  • During the absolute refractory period no second impulse is possible (Na+ channels inactivated); myelinated fibres conduct fast by saltatory conduction.
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Overview

An action potential is a rapid, short-lived change in membrane voltage that travels along a nerve or muscle fibre. It is how nerves carry information.

It lasts about 1 millisecond in a large nerve fibre and has the same size every time it fires.

Read membrane potential and ion channels first if you need the basics.

Phases of the action potential

PhaseWhat happensChannels
RestingMembrane polarised at about −70 to −90 mVK+ leak channels
DepolarisationVoltage rises rapidly and overshoots to about +35 mVVoltage-gated Na+ channels open; Na+ rushes in
RepolarisationVoltage falls back towards restNa+ channels inactivate; voltage-gated K+ channels open; K+ flows out
After-hyperpolarisationVoltage briefly dips below the resting levelK+ channels stay open a little too long

The membrane then returns to rest. The Na-K pump restores the small amounts of ions moved, but it is not needed for each action potential.

High-yield

The upstroke is caused by Na+ entry; the downstroke by K+ exit.

Positive feedback

Depolarisation opens Na+ channels; the Na+ entry causes more depolarisation, which opens more channels. This positive feedback makes the upstroke explosive.

Threshold and the all-or-none law

A stimulus must depolarise the membrane to a critical level, the threshold, for an action potential to start. In large nerve fibres, threshold is reached when the potential rises by about 15–30 mV (to around −65 mV).

  • A subthreshold stimulus produces only a small local response that fades.
  • A threshold or stronger stimulus produces a full action potential.

This is the all-or-none law. A stronger stimulus does not make a bigger action potential; it makes more frequent action potentials.

Accommodation

If the membrane is depolarised slowly, Na+ channels inactivate before threshold is reached, and no action potential fires. This is accommodation.

Refractory periods

PeriodTimingWhyEffect
AbsoluteFrom the start of the action potential to about one third of the way through repolarisationNa+ channels are inactivated and cannot reopenNo stimulus, however strong, can fire a second action potential
RelativeFollows the absolute period, during late repolarisation and after-hyperpolarisationSome Na+ channels have recovered; K+ channels still openA stronger than normal stimulus can fire
High-yield

The absolute refractory period is due to inactivation of voltage-gated Na+ channels. It limits how often a nerve can fire and makes the impulse travel in one direction.

Propagation and conduction velocity

An action potential at one point depolarises the membrane next to it through local currents, so it spreads along the fibre.

Factors that increase conduction velocity

  • Larger fibre diameter: less internal resistance.
  • Myelination.
  • Higher temperature (within normal limits).

Saltatory conduction

In myelinated fibres, the myelin sheath insulates the axon. Ion channels cluster at the nodes of Ranvier, gaps in the myelin about every 1–3 mm. The action potential jumps from node to node.

  • It increases speed by 5 to 50 times.
  • It saves energy, because ions move only at the nodes.
FibreMyelinApprox. velocity
Large myelinated (Aα)ThickUp to about 120 m/s
Small unmyelinated (C)NoneAbout 0.5–2 m/s
Exam trap

Conduction velocity depends on diameter and myelin, not on the strength of the stimulus.

Effects of electrolyte disturbances

ChangeEffectWhy
HypocalcaemiaNerves become more excitable: tingling, muscle spasm, tetanyCa2+ normally binds near Na+ channels and stabilises them; low Ca2+ lets them open more easily (threshold falls)
HypercalcaemiaNerves and muscle less excitable: weakness, constipationNa+ channels are stabilised further
HyperkalaemiaDepolarised resting potential; at first more excitable, then Na+ channels inactivate and cells fail to fireSmaller K+ gradient
HypokalaemiaHyperpolarised; less excitable; muscle weaknessLarger K+ gradient
High-yield

Low calcium makes nerves hyperexcitable (tetany, Trousseau and Chvostek signs), because Ca2+ normally raises the threshold of Na+ channels.

Excitability terms

  • Rheobase: the smallest stimulus strength that can fire the nerve if applied long enough.
  • Chronaxie: the time needed for a stimulus of twice the rheobase to fire the nerve. It is a measure of excitability.

Clinical relevance

Local anaesthetics

How it happens: drugs such as lidocaine block voltage-gated Na+ channels.

What you see: action potentials cannot start or spread, so pain sensation is blocked. Small, unmyelinated pain fibres are usually blocked first.

Demyelinating diseases

How it happens: loss of myelin in multiple sclerosis (central) or Guillain-Barré syndrome (peripheral).

What you see: slowed or blocked conduction, with weakness, numbness or visual loss depending on the nerves affected.

Tetany

How it happens: low plasma calcium (after thyroid surgery with parathyroid injury, vitamin D deficiency) or alkalosis (which lowers ionised calcium).

What you see: tingling around the mouth and fingers, carpopedal spasm, laryngeal spasm.

Exam focus

Questions ask which channel causes each phase, the all-or-none law, what happens during absolute vs relative refractory periods, the basis of saltatory conduction, the factors that change conduction velocity, why hypocalcaemia causes tetany, and how local anaesthetics work.

Quick revision

  • Upstroke: Na+ in. Downstroke: K+ out. After-hyperpolarisation: slow K+ channel closure.
  • Threshold reached → full action potential (all-or-none); stronger stimulus → higher frequency.
  • Absolute refractory: Na+ channels inactivated. Relative: stronger stimulus needed.
  • Speed rises with diameter and myelin; saltatory conduction at nodes of Ranvier.
  • Hypocalcaemia: hyperexcitable nerves, tetany.
  • Local anaesthetics block voltage-gated Na+ channels.

Written by The House Job from standard physiology references (Guyton and Hall Textbook of Medical Physiology; BRS Physiology).

FAQ

What causes the depolarisation phase of the action potential?

The opening of voltage-gated sodium channels, which lets Na+ rush into the cell.

What is the all-or-none law?

Once threshold is reached, an action potential fires at full size; below threshold, none fires.

Why does hypocalcaemia cause tetany?

Low calcium lowers the threshold of sodium channels, so nerves fire spontaneously.

What is saltatory conduction?

Conduction in myelinated fibres in which the action potential jumps from one node of Ranvier to the next.