Action potential

views updated May 18 2018

Action potential

Resources

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 of70mV 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): 791793.

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):518.

OTHER

National Alzheimers Association, 919 North Michigan Avenue, Suite 1100, Chicago, IL 606111676. (800) 2723900. August 21, 2000. <http://www.alz.org>. (accessed January 18, 2003).

K. Lee Lerner

action potentials

views updated May 18 2018

action potentials govern our lives. These are the electrical signals that are transmitted along our nerve and muscle fibres. They are essential for the communication of information to, from, and within the brain. Your ability to read this page and to understand its message, to laugh and cry, to think and feel, to see and hear, and to move your muscles, depends on action potentials.

Each action potential (also called an impulse or ‘spike’) is a transient change in the voltage (electrical potential) across the cell membrane. In nerve fibres, action potentials are brief (lasting less than 1 millisecond) and are said to be ‘all-or-nothing’, because they always have pretty much the same amplitude (voltage change), regardless of the intensity of the stimulus that sets them off. Without the capacity to produce these voltage pulses, a nerve could not transmit information over more than a very short distance, because they are such poor electrical conductors that a voltage change at one point rapidly decays as it spreads away from that point. Action potentials are, therefore, essential for signals to be sent over long distances without loss. The use of all-or-nothing pulses means that information has to be coded in digital form (in terms of the frequency of the impulses) rather than in analogue form (variation in amplitude). The frequency of nerve impulses varies with the signal strength — for example, with the intensity of sound in the case of the auditory nerves, or with the amount of pressure on the skin for cutaneous nerve fibres. The stronger the stimulus, the greater the number of action potentials per second, up to a normal maximum of a few hundred per second. A similar strategy (frequency coding rather than amplitude coding) is used by engineers to send light signals along fibre optic cables.

All cells, including nerve and muscle cells, have an electrical gradient across their cell membranes, with the inside of the cell being negative with respect to the outside at rest. This is known as the resting potential, and it is due to the unequal distribution of salts in the intracellular and extracellular fluids. Potassium ions are more concentrated inside the cell, while sodium ions are higher in concentration outside. Left to themselves, these ion concentrations would tend to equalize out: if the cell membrane were to be punctured, potassium would diffuse out of the cell, while sodium would move in, until eventually their intracellular and extracellular concentrations would equilibrate. This does not happen, however, because the cell membrane itself is impermeable to ions like sodium and potassium. Instead, the movement of ions across the membrane is restricted to tiny pores, known as ion channels, whose opening and closing is tightly controlled. At rest, the sodium channels are closed, but some potassium channels are open. Potassium ions therefore tend to move out of the cell down their concentration gradient, and because they are positively charged, this makes the inside of the cell around 70–80 mV more negative than the outside. The whole system is then roughly in balance, because the negativity inside tends to resist further efflux of potassium ions. There is, however, a very slight leakage of sodium ions into the cell. Over the long run, this is opposed by so-called sodium pumps — protein molecules in the membrane that use energy to push sodium ions out of the cell, in exchange for potassium ions moving in. This quite complex equilibrium is, then, the origin of the resting potential.

By the beginning of the twentieth century, physiologists had discovered that the action potential involves a temporary reversal of the electrical gradient across the nerve cell membrane — the inside of the cell rapidly becomes positive (depolarization) and then equally rapidly reverts to its negative resting state (repolarization). Studies of the giant axon of the squid (the motor nerve that connects to the muscles of propulsion), by Alan Hodgkin and Andrew Huxley in the Marine Biological Laboratories at Plymouth, England, in the 1940s, showed that this is due to time-dependent changes in the permeability of the cell membrane to sodium and potassium ions. World War II broke out before they could write up their results and it was not until 1952 that they published a series of seminal papers that were to win them the Nobel Prize in 1963. Subsequently, a new technique (patch clamping), invented by the German physiologists Erwin Neher and Bert Sakmann (also Nobel Prize winners, in 1991), provided insight into the molecular actions of the ion channels that underlie the action potential.

Action potentials can be triggered by any local depolarization of a nerve that exceeds a certain threshold (usually about 10 mV but sometimes up to 50 mV). In the laboratory, brief electrical stimulation can be employed to set off an action potential at any point in a nerve or muscle fibre. However, in normal circumstances, impulses are usually initiated only in sense organs and in the axon hillock — the point at which the nerve axon emerges from the cell body of a neuron. In sensory receptors, physical or chemical stimulation triggers changes in the membrane that result in local depolarization. In the cell body, depolarization occurs when an excitatory neurotransmitter is released by the terminals of nerve fibres ending in synapses on the cell. The local depolarization directly influences specialized ion channels, producing an initial opening of ‘voltage-gated’ sodium channels, followed shortly afterwards by opening of voltage-gated potassium channels. Because the sodium channels open more quickly than the potassium channels there is an initial inward flow of sodium ions. The positive charge that they carry produces a further membrane depolarization, which activates additional sodium channels, so depolarizing the membrane even further. This explosive reaction causes the rapid initial phase of the impulse, reversing the internal potential.

The amplitude of the action potential (which is typically more than a tenth of a volt) is limited by two processes. First, the sodium channels enter a specialized closed state known as the inactivated state, which curtails the depolarizing flow of sodium ions. Secondly, voltage-gated potassium channels open and the resulting outward potassium current returns the membrane potential to its resting level. The changes in potential that make up an action potential involve the movement of very small numbers of sodium and potassium ions, but, in the long run, the ion concentration gradients would degrade unless restored by the sodium–potassium pump.

Other kinds of ions, flowing through their own specialized channels, may contribute to the action potentials of nerve and muscle fibres. For example, calcium entry plays a part in the action potentials of heart muscle, and chloride flow is important in the electrical activity of skeletal muscle. As might be expected, mutations in the genes that encode ion channel proteins produce a range of nerve and muscle diseases in man. These include epilepsy, cardiac conduction abnormalities, and the muscle disorders known as myotonias.

Nerve axons come in two varieties: myelinated and unmyelinated. Myelin is a fatty sheath that surrounds the myelinated fibres and allows faster transmission of nerve impulses. Action potentials race along myelinated nerve fibres at rates of up to 100 metres/second or more, but can barely manage 1 metre/second in many unmyelinated fibres. The rate at which action potentials are transmitted also depends on temperature, and conduction slows down when the nerve is cooled. This explains why your fingers have difficulty in buttoning your jacket on a frosty morning and why ‘cold-blooded’ animals like insects and lizards, which do not maintain a constant body temperature, move around more slowly in the cold.

Frances Ashcroft

Bibliography

Hodgkin, A. L. (1963). The conduction of the nervous impulse. Liverpool University Press.


See also sensory receptors; refractory period; synapse.

Action Potential

views updated May 14 2018

Action potential

Action potentials are the electrical pulses that allow the transmission of information within nerves. An action potential represents a change in electrical potential from the resting potential of the neuronal cell membrane , and involves a series of electrical and underlying chemical changes that travel down the length of a neural cell (neuron ). The neural impulse is created by the controlled development of action potentials that sweep down the body (axon) of a neural cell.

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 compliment each other. Although long duration effects are achieved through endocrine hormonal regulation, the nervous system allows nearly immediate control, especially regulation of homeostatic mechanisms (e.g., blood pressure regulation).

The neuron cell structure 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 are transformed into action potentials that are then transmitted in a "one-way" direction (unidirectional propagation) down the axon.

In neural cells, 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 are a greater number of negatively charged proteins on the inside of the cell, and unequal distribution of cations (positively charged ions) on both sides of the cell membrane. Sodium ions (Na+) are, for example, much more numerous on the outside of the cell than on the inside. The normal distribution of charge represents the resting membrane potential (RMP) of a cell. Even in the rest state there is a standing potential across the membrane and, therefore, the membrane is polarized (contains an unequal distribution of charge). The inner cell membrane is negatively charged relative to the outer shell membrane. This potential difference can be measured in millivolts (mv or mvolts). 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 he 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 −70mv.

The structure of the cell membrane, and a process termed the sodium-potassium pump maintains 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 −70mv to +30mv. This change of approximately 100mv is an action potential that then travels down the neuron like a wave, altering the RMP as it passes.

The creation of an action potential is an "all or none" 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 done their concentration gradients to reach what is termed threshold stimulus and then generate an action potential.

The action potential is characterized by three specialized phases described as depolarization, repolarization, and hyperpolarization. During depolarization, the 100mv electrical potential change occurs. During depolarization, the neuron cannot react to additional stimuli and 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 continues loss of potassium ion form 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 speed 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 next synapse in the neural pathway). The synapse is the gap or intercellular space between neurons. The arrival of the action potential causes the release of ions and chemicals (neurotransmitters) that travel across the synapse and act as the stimulus to create 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 hall, john e. 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

cowan, w.m., d.h. harter, and e.r. kandel. "the emergence of modern neuroscience: some implications for neurology and psychiatry." annual review of neuroscience 23:343–39.

sah r., r.j. ramirez, g.y. oudit, et al. "regulation of cardiacexcitation-contraction coupling by action potential repolarization: role of the transient outward potassium current." j. physiology (jan. 2003):5–18.


organizations

national alzheimer's association, 919 north michigan avenue, suite 1100, chicago, il 60611–1676. (800) 272–3900. (august 21, 2000) [cited january 18, 2003]. <http://www.alz.org>.


K. Lee Lerner

Action Potential

views updated May 21 2018

Action potential

A momentary electrical event occurring through the membrane of a nerve cell fiber in response to a stimulus, forming a nerve impulse.

An action potential is transmitted along a nerve fiber as a wave of changing electrical charge. This wave travels at a speed that ranges from about five feet (1.5 m) per second to about 350 feet (107 m) per second, depending on various properties of the nerve fiber involved and other factors.

An action potential occurs in about one millisecond. During an action potential, there is a change in voltage across the nerve cell membrane of about 120 millivolts, and the negative electrical charge inside the resting nerve cell is reversed to a positive electrical charge. This change in voltage and reversal of electrical charge results from the movement of sodium ions, which carry a positive charge, into the nerve cell fiber. This is followed by the movement of potassium ions, which also carry a positive charge, out of the nerve cell fiber, allowing the nerve cell to return to its resting state. The temporarily increased permeability of the nerve cell fiber membrane, first to sodium ions and then to potassium ions, is caused by a chemical transmitter substance.

Further Reading

Adams, Raymond. Principles of Neurology. New York: McGraw-Hill, 1993.

action potential

views updated May 23 2018

action potential The change in electrical potential that occurs across a plasma membrane during the passage of a nerve impulse. As an impulse travels in a wavelike manner along the axon of a nerve, it causes a localized and transient switch in electric potential across the membrane from –60 mV (millivolts; the resting potential) to +45 mV. The change in electric potential is caused by an influx of sodium ions. Nervous stimulation of a muscle fibre has a similar effect.

action potential

views updated May 21 2018

action potential Change that occurs in the electrical potential between the outside and the inside of a nerve fibre or muscle fibre when stimulated by the transmission of a nerve impulse. At rest, the fibre is electrically negative inside and positive outside. When the nerve or muscle is stimulated, the charges are momentarily reversed.

action potential

views updated May 21 2018

action potential (ak-shŏn) n. the change in voltage that occurs across the membrane of a nerve or muscle cell when a nerve impulse is triggered.

action potential

views updated Jun 08 2018

action potential See ALL-OR-NOTHING LAW.