Action potential

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Action potentials are electrochemical pulses that transmit information along nerves. An action potential is a temporary change in electrical potential of a neural cell membrane (the voltage between the interior of the cell and the exterior) from the resting potential. It involves a series of electrical and underlying chemical changes that travel down the length of a neuron. An action potential is a controlled, temporary shift in the concentrations of charged molecules in the cell that sweeps rapidly down a long, fiber-like projection (axon).

There are two major control and communication systems in the human body, the endocrine system and the nervous system. In many respects, the two systems complement each other. Although long-duration effects are achieved through endocrine hormonal regulation, the nervous system allows rapid control, especially of muscles and of homeostatic mechanisms (e.g., blood pressure regulation). The cells transmitting and processing information in the nervous system are the neurons.

The neuron is specialized so that at one end, there is a flared structure termed the dendrite. At the dendrite, the neuron is able to process chemical signals from other neurons and endocrine hormones. If the signals received at the dendritic end of the neuron are of a sufficient strength and properly timed, they trigger action potentials that are then transmitted one-way (unidirectional) down the axon, primarily to the dendrites of other neurons.

In neurons, electrical potentials are created by the separation of positive and negative electrical charges that are carried on ions (charged atoms) across the cell membrane. There is unequal distribution of anions (negatively charged ions) and cations (positively charged ions) on the inside and outside of the cell membrane. Sodium ions (Na+) are, for example, more numerous on the outside of the cell than on the inside. The normal distribution of charge represents the resting membrane potential (RMP) of the cell. In the rest state there is a standing potential across the membrane; that is, the cell membrane is polarized (there is a voltage difference between the two sides of the membrane). The inner side of the cell membrane is negatively charged relative to the outer side. This potential difference can be measured in millivolts (mV). Measurements of the resting potential in a normal cell average about 70 mV.

The standing potential is maintained because, although there are both electrical and concentration gradients (a range of high to low concentration) that induce the excess sodium ions to attempt to try to enter the cell, the channels for passage are closed and the membrane remains almost impermeable to sodium ion passage in the rest state.

The situation is reversed with regard to potassium ion (K+) concentration. The concentration of potassium ions is approximately 30 times greater on the inside of the cell than on the outside. The potassium concentration and electrical gradient forces trying to move potassium out of the cell are approximately twice the strength of the sodium ion gradient forces trying to move sodium ions into the cell. Because, however, the membrane is more permeable to potassium passage, the potassium ions leak through the membrane at a greater rate than sodium enters. Accordingly, there is a net loss of positively charges ions from the inner part of the cell membrane, and the inner part of the membrane carries a relatively more negative charge than the outer part of the cell membrane. These differences result in the net RMP of –70 mV.

The structure of the cell membrane, and a process termed the sodium-potassium pump, maintain the neural cell RMP. Driven by an ATPase enzyme, the sodium potassium pump moves three sodium ions from the inside of the cell for every two potassium ions that it brings back in. The ATPase is necessary because this movement or pump of ions is an active process that moves sodium and potassium ions against the standing concentration and electrical gradients. Equivalent to moving water uphill against a gravitational gradient, such action requires the expenditure of energy to drive the appropriate pumping mechanism.

When a neuron is subjected to sufficient electrical, chemical, or in some cases physical or mechanical stimulus that is greater than or equal to a threshold stimulus, there is a rapid movement of ions, and the resting membrane potential changes from –70 mV to about +40 or +30 mV. This change of approximately 100 mV is an action potential. In each portion of the axon, molecular ion pumps in the membrane restore the resting potential quickly so that the action potential travels down the neuron like a wave, altering the RMP as it passes.

The creation of an action potential is an all-or-nothing event. Accordingly, there are no partial action potentials. The stimulus must be sufficient and properly timed to create an action potential. Only when the stimulus is of sufficient strength will the sodium and potassium ions begin to migrate down their concentration gradients to reach what is termed threshold stimulus and then generate an action potential.

The action potential is characterized by three phases described as depolarization, repolarization, and hyperpolarization. During depolarization, the 100 mV potential change occurs. During depolarization, the neuron cannot react to additional stimuli; this inability is termed the absolute refractory period. Also during depolarization, the RMP of→70mV is reestablished. When the RMP becomes more negative than usual, this phase is termed hyperpolarization. As repolarization proceeds, the neuron achieves an increasing ability to respond to stimuli that are greater than the threshold stimulus, and so undergoes a relative refractory period.

The opening of selected channels in the cell membrane allows the rapid movement of ions down their respective electrical and concentration gradients. This movement continues until the change in charge is sufficient to close the respective channels. Because the potassium ion channels in the cell membrane are slower to close than the sodium ion channels, however, there is a continual loss of potassium ion from the inner cell that leads to hyperpolarization. The sodium-potassium pump then restores and maintains the normal RMP.

In demyelinated nerve fibers, the depolarization induces further depolarization in adjacent areas of the membrane. In myelinated fibers, a process termed salutatory conduction allows transmission of an action potential, despite the insulating effect of the myelin sheath. Because of the sheath, ion movement takes place only at the Nodes of Ranvier. The action potential jumps from node to node along the myelinated axon. Differing types of nerve fibers exhibit different speeds of action potential conduction. Larger fibers (also with decreased electrical resistance) exhibit faster transmission than smaller diameter fibers).

The action potential ultimately reaches the presynaptic portion of the neuron, the terminal part of the neuron adjacent to the synapse. A synapse is a gap or fluid-filled intercellular space between neurons. The arrival of the action potential causes the release of ions and chemicals (neurotransmitters) that diffuse across the synapse and act as the stimulus which may, if combined with other stimuli, trigger another action potential in the next neuron.

See also Adenosine triphosphate; Nerve impulses and conduction of impulses; Neuromuscular diseases; Reflex; Touch.

Resources

BOOKS

Guyton, Arthur C., and John E. Hall. Textbook of Medical Physiology. 10th ed. Philadelphia: W. B. Saunders Co., 2000.

Kandel, E. R., J. H. Schwartz, and T. M. Jessell, eds. Principles of Neural Science. 4th ed. Boston: Elsevier, 2000.

Thibodeau, Gary A., and Kevin T. Patton. Anatomy & Physiology. 5th ed. St. Louis: Mosby, 2002.

PERIODICALS

Bullock, Theodore H., et al. “The Neuron Doctrine, Redux.” Science. 310 (2005): 791–793.

Patolsky, F., et al. “Detection, Stimulation, and Inhibition of Neuronal Signals with High-Density Nanowire Transistor Arrays.” Science. 313 (2006): 1100-1104.

Sah R., R. J. Ramirez, G. Y. Oudit, et al. “Regulation of Cardiac Excitation-Contraction Coupling By Action Potential Repolarization: Role of the Transient Outward Potassium Current.” Journal of Physiology (January 2003):5–18.

OTHER

National Alzheimer’s Association, 919 North Michigan Avenue, Suite 1100, Chicago, IL 60611–1676. (800) 272–3900. August 21, 2000. <http://www.alz.org>. (accessed January 18, 2003).

K. Lee Lerner