Action Potentials: Generation and Propagation


All cells maintain a voltage across their plasma membranes. However, only excitable cells can generate action potentials, the rapid transient changes in membrane potential that spread along the surface of these unique cells. Action potential generation and propagation occur through and is regulated by, the function of voltage‐gated ion channels. These channels are proteins with ion‐selective pores that span the cell membrane. Ion channels undergo changes in their structural conformation in response to changes in the electrical field across the membrane. These structural changes cause the opening of the channels' pores through which ions can flow down their electrochemical gradient. The charge carried by ions creates an electrical current and rapidly alters the membrane potential with time and voltage‐dependent properties. This rapid, transient membrane potential change is called the action potential. Action potentials transmit information within neurons, trigger contractions within muscle cells, and lead to exocytosis in secretory cells.

Key Concepts

  • Rapid changes in membrane ion permeabilities generate action potentials.
  • Ion channels are transmembrane proteins that control the passage of ions. Voltage‐gated sodium ion channels play a crucial role in the development of action potential.
  • Action potential is ‘all or none’ response.
  • Refractory Period is the time when it is physiologically impossible to elicit another action potential.
  • Action potential propagation changes in a ‘day/night’ dependent manner ‘circadian rhythm’.

Keywords: action potential; ion channels; refractory period; circadian rhythm; depolarisation; repolarisation; ionic currents

Figure 1. Electrochemical gradients arise from unequal distributions of ions across cell membranes. Ionic concentrations shown here are approximations of physiological conditions. Weight of arrow shows relative electrochemical driving force.
Figure 2. Voltage‐dependent gating of ion channels. Voltage‐gated channels change their conformational state from closed to open to inactivated in response to depolarisation. When open, ions can flow through the channels.
Figure 3. Ionic basis of the action potential. Top trace shows the voltage recording during the action potential, with relative positions along the voltage axis of Vrest, threshold potential, EK, ENa, and, as a reference point, 0 mV. Middle trace shows Na+ conductance during the action potential. Bottom trace shows K+ conductance during the action potential. Note the overlap between the increase in K+ conductance and the after‐hyperpolarisation.
Figure 4. Equivalent circuit of an axon showing the essential features for the basis of cable properties. RM, membrane resistance; RO, extracellular resistance; RI, intracellular resistance; CM, membrane capacitance.
Figure 5. Electrotonic decay of voltage along a nonmyelinated (a) and a myelinated (b) axon. Note that the voltage deflection caused by the same influx of Na+ is larger in a myelinated axon because of higher effective membrane resistance. Also note that the length constant (l) is greater in the myelinated axon so the local currents travel farther within the axon.


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Fouda, Mohamed A, and Ruben, Peter C(Jul 2020) Action Potentials: Generation and Propagation. In: eLS. John Wiley & Sons Ltd, Chichester. [doi: 10.1002/9780470015902.a0000278.pub3]