Action Potentials: Generation and Propagation

Csilla Egri, Simon Fraser University, Burnaby, British Columbia, Canada
Peter C Ruben, Simon Fraser University, Burnaby, British Columbia, Canada

Published online: April 2012

DOI: 10.1002/9780470015902.a0000278.pub2

Full Article on Wiley Online Library

All cells maintain a voltage across their plasma membranes. Only excitable cells, however, 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 occurs through, and is regulated by, the function of voltage‐gated ion channels – 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 pores – channels – 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:

All cells maintain a voltage difference across their plasma membranes.
Action potentials are all‐or‐nothing, transient changes in membrane potentials of electrically excitable cells that carry important cellular information.
Influx of sodium ions through voltage‐gated sodium channels is responsible for the upstroke of the action potential, whereas efflux of potassium ions through voltage‐gated potassium channels is responsible for the falling phase.
Propagation of action potentials depends on gating kinetics of ion channels and intracellular and membrane resistances.

Keywords: membrane potential; ionic current; threshold; refractoriness; length constant

	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 a Na⁺ channel. 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 an action potential, with relative positions along the voltage axis of V_rest, threshold potential, E_K, E_Na, 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 K⁺ conductance increase and the after‐hyperpolarisation.
	Figure 4. Equivalent circuit of an axon showing the essential features for the basis of cable properties. R_M, membrane resistance; R_O, extracellular resistance; R_I, intracellular resistance; C_M, membrane capacitance.
	Figure 5. Electrotonic decay of voltage along a nonmyelinated (top) and a myelinated (bottom) 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 (λ) is greater in the myelinated axon so the local currents travel farther within the axon.

References
	Adrian RH, Chandler WK, Hodgkin AL et al. (1970) Slow changes in potassium permeability in skeletal muscle. Journal of Physiology 208(3): 645–668.
	Bezanilla F (2008) How membrane proteins sense voltage. Nature Reviews Molecular Cell Biology 9(4): 323–332.
	Catterall WA, Goldin AL and Waxman SG (2005) International Union of Pharmacology. XLVII. Nomenclature and structure‐function relationships of voltage‐gated sodium channels. Reviews of Pharmacology 57(4): 397–409.
	Frankenhauser B (1952) Saltatory conduction in myelinated nerve fibres. Journal of Physiology 118(1): 107–112.
	Gutman GA, Chandy KG, Grissmer S et al. (2005) International Union of Pharmacology. LIII. Nomenclature and molecular relationships of voltage‐gated potassium channels. Reviews of Pharmacology 57(4): 473–508.
	Kellenberger S, Scheuer T and Catterall WA (1996) Movement of the Na⁺ channel inactivation gate during inactivation. Journal of Biological Chemistry 271(48): 30971–30979.
	Poulter MO and Padjen AL (1995) Different voltage‐dependent potassium conductances regulate action potential repolarisation and excitability in frog myelinated axon. Neuroscience 68(2): 497–504.
Further Reading
	ePath Bezanilla F (2006) Electrophysiology and the Molecular Basis of Electrical Excitability [http://pb010.anges.ucla.edu].
	book Hille B (2001) Ion Channels of Excitable Membranes, 3rd edn, chaps. 2 and 3. Sunderland, MA: Sinauer.
	book Kandel ER, Schwartz JH and Jessel TM (1991) Principles of Neural Science, 4th edn, chaps. 6–9. New York: Elselvier.
	book Kew JNC and Davies CH (2010) Ion Channels: From Structure to Function, chaps. 2.1 and 2.3. New York: Oxford University Press.
	book Levitan IB and Kaczmarek LK (2002) The Neuron: Cell and Molecular Biology, 3rd edn, chaps. 3–5. Oxford: Oxford University Press.
	book Nicholls JG, Martin AR and Wallace BG (2001) From Neuron to Brain, 4th edn, chaps. 2–5. Sunderland, MA: Sinauer.
	book Purves D, Augustine GJ, Fitzpatrick D et al. (2004) Neuroscience, 3rd edn, chaps. 2–4. Sunderland, MA: Sinauer.
	book Shepherd GM (1994) Neurobiology, 3rd edn, chaps. 4 and 5. Oxford: Oxford University Press.

Article Title:	Action Potentials: Generation and Propagation
* Name:
* E-mail:
* Note:

Action Potentials: Generation and Propagation

Key Concepts:

Related Sub-Topics: