Membrane Potential and the Action Potential

How animal cells store electrical energy as a voltage across their membrane, and how excitable cells use that voltage to fire and conduct the all-or-none nerve impulse.

Definition

The membrane potential is the voltage difference across a cell's plasma membrane set by ion gradients and selective permeability; the action potential is a brief, regenerative, all-or-none reversal of that potential produced by the sequential opening and closing of voltage-gated ion channels in an excitable cell.

Scope

This topic covers the origin of the resting membrane potential, the ion gradients and selective channels that produce it, and the sequence of voltage-gated events that generate, propagate, and terminate the action potential. It treats the Nernst and constant-field descriptions of equilibrium and reversal potentials, the Hodgkin–Huxley account of Na+ and K+ conductances, threshold and refractoriness, and the continuous versus saltatory conduction of impulses. Material is presented as comparative-physiology reference, not as clinical electrophysiology.

Core questions

• Why is the inside of a resting cell electrically negative relative to the outside?
• What ionic movements produce the rising and falling phases of the action potential?
• What sets the threshold for firing and why is there a refractory period?
• How does the impulse travel along an axon, and why is myelinated conduction faster?

Key theories

Hodgkin–Huxley conductance model

Voltage-clamp measurements showed that the action potential results from time- and voltage-dependent Na+ and K+ conductances, which can be combined into equations that reproduce the impulse waveform and its propagation.

Constant-field treatment of resting and reversal potentials

When several permeant ions contribute, the membrane potential is given by the Goldman–Hodgkin–Katz equation, which weights each ion's equilibrium potential by its relative permeability under a constant electric field.

Mechanisms

At rest, the Na+/K+-ATPase maintains high internal K+ and high external Na+, and the membrane's dominant K+ permeability holds the potential near the K+ equilibrium value. A suprathreshold depolarisation opens voltage-gated Na+ channels, whose inward current drives the membrane toward the Na+ equilibrium potential (the spike). Na+ channels then inactivate while delayed-rectifier K+ channels open, repolarising and briefly hyperpolarising the cell; inactivation imposes absolute and relative refractory periods that enforce one-way propagation. Local circuit currents spread depolarisation to adjacent membrane; in myelinated axons this is restricted to nodes of Ranvier, producing rapid saltatory conduction.

Clinical relevance

The voltage-clamp framework derived from invertebrate axons explains how local anaesthetics, neurotoxins, and antiarrhythmic and antiepileptic agents act on voltage-gated channels; it remains a foundation for interpreting excitable-tissue physiology. This is an educational reference and not medical guidance.

History

Building on the squid giant axon preparation, Hodgkin and Huxley recorded the intracellular action potential in 1939 and, using the voltage clamp, produced their quantitative conductance model in 1952 — a landmark recognised with a Nobel Prize. Goldman's 1943 constant-field equation supplied the multi-ion description of the resting potential that the spike sits upon.

Key figures

• Alan Hodgkin
• Andrew Huxley
• David Goldman
• Walther Nernst

Seminal works

• hodgkinhuxley1952
• goldman1943
• hill2016

Frequently asked questions

What does 'all-or-none' mean for an action potential?

Once a stimulus pushes the membrane past threshold, the impulse fires at full amplitude regardless of how strong the stimulus was; weaker stimuli simply fail to trigger it.

Why does myelin speed up conduction?

Myelin insulates stretches of axon so the regenerating current jumps between the unmyelinated nodes of Ranvier, a process called saltatory conduction that is much faster than continuous spread.