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Action potential

As the traveling signals of nerves and as the localized changes that contract muscle cells, action potentials are an essential feature of animal life. They set the pace of thought and action, constrain the sizes of evolving anatomies and enable centralized control and coordination of organs and tissues. Action potentials may also be used in internal communication of plants.


Basic features

When a biological cell or patch of membrane undergoes an action potential—or electrical excitation—the polarity of the transmembrane voltage swings rapidly from negative to positive and back. Within any one excitable cell, consecutive action potentials typically are indistinguishable. Also between different cells the amplitudes of the voltage swings tend to be roughly the same. But the speed and simplicity of action potentials vary significantly between cells, in particular between different cell types.

Minimally, an action potential involves a depolarization, a repolarization and finally a hyperpolarization (or "undershoot"). In specialized muscle cells of the heart, such as the pacemaker cells, a plateau phase of intermediate voltage may precede repolarization.

Underlying mechanism

The transmembrane voltage changes that take place during an action potential result from changes in the permeability of the membrane to specific ions, the internal and external concentrations of which cells maintain in an imbalance. In the axon fibers of nerves, depolarization results from the inward rush of sodium ions, while repolarization and hyperpolarization arise from an outward rush of potassium ions. Calcium ions make up most or all of the depolarizing currents at an axon's presynaptic terminus, in muscle cells (including the heart's) and in some dendrites.

The imbalance of ions that makes possible not only action potentials but the resting cell potential arises through the work of pumps, in particular the sodium-potassium exchanger. While the cell is at resting cell potential the electric forces between the sodium and potassium of the neuron is counterbalanced by the "diffusive forces," creating a state of equilibrium.

Changes in membrane permeability and the onset and cessation of ionic currents reflect the opening and closing of voltage-gated ion channels, which provide portals through the membrane for ions. Residing in and spanning the membrane, these proteins sense and respond to changes in transmembrane potential.

The depolarization phase of an action potential is due to the opening of voltage-gated ion channels, either sodium channels or calcium channels or a combination of both, depending on the particular membrane. Sodium ions and calcium ions are positively charged. When a voltage-gated sodium channel or calcium channel opens, positively charged ions move into the cell. Voltage-gated sodium channels automatically gate shut after about a millisecond. Calcium-mediated action potentials can be much longer in duration. The repolarization phase of an action potential is due to the opening of voltage-gated potassium channels. Cells normally keep the concentration of potassium ions high inside cells. When voltage-gated potassium channels open, positively charged potassium ions move out of the cell, causing the membrane potential to return to a negative inside potential.


Action potentials are triggered by an initial depolarization to the point of threshold. This threshold potential varies but generally is about 15 millivolts above the resting potential of the cell. Action potential initiation occurs at a region called the axon hillock, a point near the base of the axon with the highest concentration of voltage gated ion channels but may occur anywhere along the axon. In his discovery of "animal electricity," Luigi Galvani elicited an action potential through contact of his scalpel with the sciatic motor nerve of a frog he was dissecting, causing one of its legs to kick as in life.

Wave propagation

In the fine fibers of simple (or unmyelinated) axons, action potentials propagate as waves, which travel at speeds up to 120 meters per second.

The propagation speed of these impulses is faster in fatter fibers than in thin ones, other things being equal. In their Nobel prize-winning work uncovering the wave nature and ionic mechanism of action potentials, Alan Hodgkin and Andrew Huxley performed experiments on the giant fiber of Atlantic squid . Responsible for initiating flight, this axon is fat enough to be seen without a microscope (100 to 1000 times larger than is typical). This is assumed to reflect an adaptation for speed. Indeed, the velocity of nerve impulses in these fibers is among the fastest in nature.

Saltatory propagation

Many neurons have insulating sheaths of myelin surrounding their axons, which enable action potentials to travel faster than in unmyelinated axons of the same diameter. The myelin sheathing normally runs along the axon in sections about 1 mm long, punctuated by unsheathed nodes of Ranvier.

Because the salty cytoplasm of the axon is electrically conductive, and because the myelin inhibits charge leakage through the membrane, depolarization at one node is sufficient to elevate the voltage at a neighboring node to the threshold for action potential initiation. Thus in myelinated axons, action potentials do not propagate as waves, but recur at successive nodes and in effect hop along the axon. This mode of propagation is known as saltatory conduction.

The disease multiple sclerosis (MS) is due to a breakdown of myelin sheathing, and degrades muscle control by destroying axons' ability to conduct action potentials.

Refractory period

Where membrane has undergone an action potential a refractory period follows, during which a second action potential is inhibited due to the reversible inactivation of ion channels. The refractory period limits the frequency with which a cell can fire, varies between cell types and can be subject to regulation by enzymes or second messengers, for example, within any given cell.

Noteworthy characteristics of the action potential

The initiation of an action potential is "all-or-none" and the subsequent wave travels by "active propagation." The same passive conduction that spreads depolarization from one node to another in a myelinated axon occurs over a shorter distance in unmyelinated cells, such that excitation in any patch of membrane will depolarize a neighborhood around it and bring it to threshhold. This "regenerates" the action potential in this neighboring region from the energy that stored in the ionic imbalance there and advances the wave. As a result, the peak amplitude of the depolarization doesn't decrease as an action potential propagates allowing it to cover distances that a passive electrical wave or signal could not. This active mode propagation is slower, however.

Detection and observation

Action potentials (APs) are measured with the recording techniques of electrophysiology. In the case of an archetypal nerve action potential on an oscilloscope, the relatively large swing to a more positive value, followed by the repolarization recovery and undershoot together trace an arc that could be described as a distorted sine wave—or like the blips on hospital EKG machines that can be seen on TV (these EKG waves are a smear of all the action potentials in one heartbeat, so they enact more slowly than any individual AP and have a somewhat more complicated shape). In an unmyelinated axon that is firing an action potential, the transmembrane potential at any instant will vary from point to point along the fiber, with its amplitude depending on whether the AP wave has reached that point or passed it, and how long ago. A recording from a single point will show the various stages of the action potential enacted—depolarization, repolarization, hyperpolarization—as the wave passes.

Detailed features

Prototypically, depolarization and repolarization together are complete in about two milliseconds, while undershoots can last hundreds of milliseconds, depending on the cell. In neurons, the exact length of the roughly two-millisecond delay in repolarization can have a strong effect on the amount of neurotransmitter released at a synapse. The duration of the hyperpolarization determines a nerve's refractory period (how long until it may conduct another action potential) and hence the frequency at which it will fire under continuous stimulation. Both of these properties are subject to biological regulation, primarily (among the mechanisms discovered so far) acting on ion channels selective for potassium.

In pacemaker and other cardiac muscle cells, inward calcium currents determine shape and duration of the plateau phase, which in turn controls the strength and duration of contraction. See cardiac action potential, ventricular action potential, atrial action potential , and pacemaker action potential for more details.


  • Bear, M.F., B.W. Conners, and M.A. Paradisa. 2001. Neuroscience: Exploring the Brain. Baltimore: Lippincott.[1]
  • Kandel, Eric, James Schwartz, and Thomas Jessel. 2000. Principles of Neural Science. 4th ed. McGraw-Hill, New York.[2]
  • Dale Purvis, et al. Neuroscience, 2nd ed. 2001. Sinauer Associates, Inc. Ion Channels Underlying Action Potentials. [3]

Last updated: 10-14-2005 16:17:20
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