Phases of the Action Potential and Hodgkin-Huxley Theory

The action potential is a stereotyped sequence of voltage changes that an excitable membrane produces once depolarisation crosses threshold. It proceeds through a rapid depolarising upstroke, an overshoot above zero, a repolarising downstroke, and often a transient hyperpolarisation, before returning to rest. The Hodgkin-Huxley theory explains this sequence quantitatively as the product of voltage- and time-dependent sodium and potassium conductances.

Definition

The action potential is a transient, regenerative reversal of membrane potential comprising a depolarising upstroke, an overshoot, a repolarising phase, and an afterhyperpolarisation; the Hodgkin-Huxley theory models these phases as the result of voltage-dependent sodium and potassium conductances described by gating variables.

Scope

This topic describes the successive phases of the action potential and the Hodgkin-Huxley framework that accounts for them. It covers the ionic basis of each phase, the gating variables that govern conductance, and how the model reproduces and predicts the impulse. It treats this as foundational physiology and electrophysiology, not as clinical guidance.

Core questions

• Which ionic currents produce the upstroke, repolarisation, and afterhyperpolarisation of the action potential?
• How do the Hodgkin-Huxley gating variables (m, h, n) capture the time course of sodium and potassium conductance?
• Why does the membrane overshoot zero and approach the sodium equilibrium potential during the upstroke?

Key concepts

• Depolarising upstroke
• Overshoot
• Repolarisation
• Afterhyperpolarisation
• Sodium and potassium conductances
• Gating variables (m, h, n)
• Equilibrium (Nernst) potentials

Key theories

Hodgkin-Huxley model

A quantitative description in which membrane current is the sum of sodium, potassium, and leak components, with conductances governed by voltage- and time-dependent gating variables; the equations reproduce the action potential, its threshold, and its conduction.

Sodium hypothesis

The proposal that the rising phase and overshoot of the action potential are produced by a transient increase in membrane permeability to sodium, driving the potential toward the sodium equilibrium potential.

Mechanisms

When depolarisation reaches threshold, voltage-gated sodium channels open rapidly; the resulting sodium influx is regenerative, depolarising the membrane further toward the sodium equilibrium potential and producing the steep upstroke and overshoot. Hodgkin and Katz first showed that the upstroke depends on extracellular sodium. Sodium channels then inactivate while voltage-gated potassium channels open more slowly, so potassium efflux repolarises the membrane; the continued potassium conductance can drive the potential transiently below rest, giving the afterhyperpolarisation. Hodgkin and Huxley separated these currents experimentally and represented each conductance with gating variables whose voltage- and time-dependence reproduced the entire phase sequence and the propagating impulse.

Clinical relevance

Understanding the ionic basis of each action-potential phase underlies the interpretation of excitability and of how altered sodium or potassium currents change firing. This entry is descriptive reference material on normal mechanism and is not a basis for individual clinical decisions.

Evidence & guidelines

The phase structure and its ionic basis derive from the Hodgkin-Huxley voltage-clamp studies on the squid giant axon and from later reviews of action potentials in mammalian neurons; these are mechanistic studies rather than clinical guidelines.

History

Following Hodgkin and Katz's 1949 demonstration that the overshoot depends on extracellular sodium, Hodgkin and Huxley used the voltage clamp on the squid giant axon to separate the sodium and potassium currents and, in 1952, to express them as a system of equations. That model reproduced the action potential's shape, threshold, refractoriness, and conduction velocity, and remains the foundation of computational neurophysiology.

Key figures

• Alan Hodgkin
• Andrew Huxley
• Bernard Katz
• Bruce Bean

Seminal works

• hodgkin-huxley-1952
• hodgkin-katz-1949
• hodgkin-huxley-1952-currents

Frequently asked questions

What causes the upstroke of the action potential?

A regenerative influx of sodium ions through rapidly opening voltage-gated sodium channels, which drives the membrane potential toward the sodium equilibrium potential.

Why is there an afterhyperpolarisation?

Voltage-gated potassium channels remain open after the membrane has repolarised, and the continued potassium efflux can briefly drive the potential below the resting level before the channels close.