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Action potential

2007 Schools Wikipedia Selection. Related subjects: General Biology

   A. A schematic view of an idealized action potential illustrates its
   various phases as the action potential passes a point on a cell
   membrane. B. Actual recordings of action potentials are often distorted
   compared to the schematic view because of variations in
   electrophysiological techniques used to make the recording
   Enlarge
   A. A schematic view of an idealized action potential illustrates its
   various phases as the action potential passes a point on a cell
   membrane. B. Actual recordings of action potentials are often distorted
   compared to the schematic view because of variations in
   electrophysiological techniques used to make the recording

   An action potential is a wave of electrical discharge that travels
   along the membrane of a cell. Action potentials are an essential
   feature of animal life, rapidly carrying information within and between
   tissues. They are also exhibited by some plants. Action potentials can
   be created by many types of cells, but are used most extensively by the
   nervous system for communication between neurons and to transmit
   information from neurons to other body tissues such as muscles and
   glands.

   Action potentials are not the same in all cell types and can even vary
   in their properties at different locations in the same cell. For
   example, cardiac action potentials are significantly different from the
   action potentials in most neurons. This article is particularly
   concerned with the "typical" action potential of axons.

Overview

   A voltage, or difference in electrostatic potential, always exists
   between the inside and outside of a cell. This results from the
   distribution of ions across the cell membrane and from the permeability
   of the membrane to these ions. The voltage of an inactive cell stays at
   a negative value (inside relative to outside the cell) and varies
   little. When the membrane of an excitable cell is depolarized beyond a
   threshold, the cell will undergo (or "fire") an action potential, often
   called a "spike" (see Threshold and initiation).

   An action potential is a rapid swing in the polarity of the voltage
   from negative to positive and back, the entire cycle lasting a few
   milliseconds. Each cycle—and therefore each action potential—has a
   rising phase, a falling phase, and finally an undershoot (see Action
   potential phases). In specialized muscle cells of the heart, such as
   cardiac pacemaker cells, a plateau phase of intermediate voltage may
   precede the falling phase, extending the action potential duration into
   hundreds of milliseconds.

   Action potentials are measured with the recording techniques of
   electrophysiology and more recently with neurochips containing EOSFETs.
   An oscilloscope recording the membrane potential from a single point on
   an axon shows each stage of the action potential as the wave passes.
   These phases trace an arc that resembles a distorted sine wave. Its
   amplitude depends on whether the action potential wave has reached that
   point on the membrane or has passed it and if so, how long ago.

   The action potential does not dwell in one location of the cell's
   membrane, but travels along the membrane (see Propagation). It can
   travel along an axon for long distances, for example to carry signals
   from the spinal cord to the muscles of the foot. In large animals, such
   as giraffes and whales, the distance traveled can be many meters.

   Both the speed and complexity of action potentials vary between
   different types of cells. However, the amplitudes of the voltage swings
   tend to be roughly the same. Within any one cell, consecutive action
   potentials typically are indistinguishable. Neurons are thought to
   transmit information by generating sequences of action potentials
   called "spike trains". By varying both the rate as well as the precise
   timing of the action potentials they generate, neurons can change the
   information that they transmit.

Underlying mechanism

   The hydrophobic cell membrane prevents charged molecules from easily
   diffusing through it, permitting a potential difference to exist across
   the membrane.
   Enlarge
   The hydrophobic cell membrane prevents charged molecules from easily
   diffusing through it, permitting a potential difference to exist across
   the membrane.

Resting potential

   The potential difference that exists across the membrane of all cells
   is usually negative inside the cell with respect to the outside. The
   membrane is said to be polarized. The potential difference across the
   membrane at rest is called the resting potential and is approximately
   -70 mV in neurons, with the negative sign indicating that the inside of
   the cell is negative with respect to the outside. The establishment of
   this potential difference involves several factors, most importantly
   the transport of ions across the cell membrane and the selective
   permeability of the membrane to these ions.

   The active transport of potassium and sodium ions into and out of the
   cell, respectively, is accomplished by a number of sodium-potassium
   pumps scattered across the cell membrane. Each pump transports two ions
   of potassium into the cell for every three ions of sodium pumped out.
   This establishes a particular distribution of positively charged ions
   across the cell membrane, with more sodium present outside the cell
   than inside, and more potassium inside the cell than outside. In some
   situations, the electrogenic sodium-potassium pumps make a significant
   contribution to the resting membrane potential, but in most cells there
   are potassium leakage channels that dominate the value of the resting
   potential.

   Sodium and potassium ions diffuse through open ion channels under the
   influence of their electrochemical gradients. At the resting potential,
   the net movement of sodium into the cell equals the net movement of
   potassium out of the cell. However, the resting cell membrane is
   approximately 75 times more permeable to potassium than to sodium, due
   to potassium leak channels that are always open. As a result, the
   cell's resting membrane potential is closer to the equilibrium
   potential of potassium (=E[K]=−90 mV) than the equilibrium potential of
   sodium (=E[Na]=+45 mV). The cell's resting potential is roughly -70 mV.

   Like the resting potential, action potentials of many neurons depend
   upon the permeability of the cell membrane to sodium and potassium
   ions.

Phases

   The sequence of events that underlie the action potential are outlined
   below:

Resting potential

   At resting potential some potassium leak channels are open but the
   voltage-gated sodium channels are closed. Potassium diffusing down the
   potassium concentration gradient creates a negative-inside membrane
   potential.

Stimulation

   A local membrane depolarization caused by an excitatory stimulus causes
   some voltage-gated sodium channels in the neuron cell surface membrane
   to open and therefore sodium ions diffuse in through the channels along
   their electrochemical gradient. Being positively charged, they begin a
   reversal in the potential difference across the membrane from
   negative-inside to positive-inside. Initially, the inward movement of
   sodium ions is also favored by the negative-inside membrane potential.

Rising phase

   As sodium ions enter and the membrane potential becomes less negative,
   more sodium channels open, causing an even greater influx of sodium
   ions. This is an example of positive feedback. As more sodium channels
   open, the sodium current dominates over the potassium leak current and
   the membrane potential becomes positive inside.

Peak

   Establishment of a membrane potential of around +30 mV closes the
   voltage-sensitive inactivation gates of the sodium channels, which are
   sensitive to the now-positive membrane potential gradient, preventing
   further influx of sodium. While this occurs, the voltage-sensitive
   activation gates on the voltage-gated potassium channels begin to open.

Falling phase

   As voltage-gated potassium channels open, there is a large outward
   movement of potassium ions driven by the potassium concentration
   gradient and initially favored by the positive-inside electrical
   gradient. As potassium ions diffuse out, this movement of positive
   charge causes a reversal of the membrane potential to negative-inside
   and repolarization of the neuron back towards the large negative-inside
   resting potential.

Undershoot

   Closing of voltage-gated potassium channels is both voltage- and
   time-dependent. As potassium exits the cell, the resulting membrane
   repolarization initiates the closing of voltage-gated potassium
   channels. These channels do not close immediately in response to a
   change in membrane potential. Rather, voltage-gated potassium channels
   (also called delayed rectifier potassium channels) is delayed. As a
   result, potassium continues to flow out of the cell even after the
   membrane has fully repolarized. Thus the membrane potential dips below
   the normal resting membrane potential of the cell for a brief moment;
   this dip of hyperpolarization is known as the undershoot.

Threshold and initiation

   A plot of current (ion flux) against voltage (transmembrane potential)
   illustrates the action potential threshold (red arrow) of an idealized
   cell.
   Enlarge
   A plot of current (ion flux) against voltage (transmembrane potential)
   illustrates the action potential threshold (red arrow) of an idealized
   cell.

   Action potentials are triggered when an initial depolarization reaches
   threshold. This threshold potential varies, but generally is about 15
   millivolts above the cell's resting membrane potential, occurring when
   the inward sodium current exceeds the outward potassium current. The
   net influx of positive charges carried by sodium ions depolarizes the
   membrane potential, leading to the further opening of voltage-gated
   sodium channels. These channels support greater inward current causing
   further depolarization, creating a positive-feedback cycle that drives
   the membrane potential to a very depolarized level.

   The action potential threshold can be shifted by changing the balance
   between sodium and potassium currents. For example, if some of the
   sodium channels are in an inactivated state, then a given level of
   depolarization will open fewer sodium channels and a greater
   depolarization will be needed to trigger an action potential. This is
   the basis for the refractory period (see Refractory period).

   Action potentials are largely dictated by the interplay between sodium
   and potassium ions (although there are minor contributions from other
   ions such as calcium and chloride), and are often modeled using
   hypothetical cells containing only two transmembrane ion channels (a
   voltage-gated sodium channel and a non-voltage-gated potassium
   channel). The origin of the action potential threshold may be studied
   using I/V curves (right) that plot currents through ion channels
   against the cell's membrane potential. (Note that the illustrated I/V
   is an "instantaneous" current voltage relationship. It represents the
   peak current through channels at a given voltage before any
   inactivation has taken place (i.e. ~ 1 ms after stepping to that
   voltage for the Na current. The most positive voltages in this plot are
   only attainable by the cell through artificial means - i.e. voltages
   imposed by the voltage-clamp apparatus).

   Four significant points in the I/V curve are indicated by arrows in the
   figure:
    1. The green arrow indicates the resting potential of the cell and
       also the value of the equilibrium potential for potassium (E[k]).
       As the K^+ channel is the only one open at these negative voltages,
       the cell will rest at E[k]. Note that a stable resting potential
       will be present at any voltage where the summed I/V (green line)
       crosses the zero current (x-axis) point with a positive slope, such
       as at the green arrow. Consider why: any perturbation of the
       membrane potential in the negative direction will result in inward
       current that will depolarize the cell back toward the crossing
       point, while, any perturbation of the membrane potential in the
       positive direction will result in an outward current that will
       hyperpolarize the cell back toward the crossing point. Thus, any
       perturbation of the membrane potential around a positive slope
       crossing will tend to return the voltage to that crossing value.
    2. The yellow arrow indicates the equilibrium potential for Na^+
       (E[Na]). In this two-ion system, E[Na] is the natural limit of
       membrane potential beyond which a cell cannot pass. Current values
       illustrated in this graph that exceed E[Na] are measured by
       artificially pushing the cell's voltage past its natural limit.
       Note however, that E[Na] could only be reached if the potassium
       current were absent.
    3. The blue arrow indicates the maximum voltage that the peak of the
       action potential can approach. This is the actual natural maximum
       membrane potential that this cell can reach. It cannot reach E[Na]
       because of the counteracting influence of the potassium current.
    4. The red arrow indicates the action potential threshold. This is
       where I[sum] becomes net-inward. Note that this is a zero-current
       crossing, but with a negative slope. Any such "negative slope
       crossing" of the zero current level in an I/V plot is an unstable
       point. At any voltage negative to this crossing, the current is
       outward and so a cell will tend to return to its resting potential.
       At any voltage positive of this crossing, the current is inward and
       will tend to depolarize the cell. This depolarization leads to more
       inward current, thus the sodium current become regenerative. The
       point at which the green line reaches its most negative value is
       the point where all sodium channels are open. Depolarizations
       beyond that point thus decrease the sodium current as the driving
       force decreases as the membrane potential approaches E[Na].

   The action potential threshold is often confused with the "threshold"
   of sodium channel opening. This is incorrect, because sodium channels
   have no threshold. Instead, they open in response to depolarization in
   a stochastic manner. Depolarization does not so much open the channel
   as increases the probability of it being open. Even at hyperpolarized
   potentials, a sodium channel will open very occasionally. In addition,
   the threshold of an action potential is not the voltage at which sodium
   current becomes significant; it is the point where it exceeds the
   potassium current.

   Biologically in neurons, depolarization typically originates in the
   dendrites at synapses. In principle, however, an action potential may
   be initiated anywhere along a nerve fibre. In his discovery of "animal
   electricity," Luigi Galvani made a leg of a dead frog kick as in life
   by touching a sciatic nerve with his scalpel, to which he had
   inadvertently transferred a negative, static-electric charge, thus
   initiating an action potential.

Circuit model

   A. A basic RC circuit superimposed on an image of a membrane bilayer
   shows the relationship between the two. B. More elaborate circuits can
   be used to model membranes containing ion channels, such as this one
   containing at channels for sodium (blue) and potassium (green).
   Enlarge
   A. A basic RC circuit superimposed on an image of a membrane bilayer
   shows the relationship between the two. B. More elaborate circuits can
   be used to model membranes containing ion channels, such as this one
   containing at channels for sodium (blue) and potassium (green).

   Cell membranes that contain ion channels can be modeled as RC circuits
   to better understand the propagation of action potentials in biological
   membranes. In such a circuit, the resistor represents the membrane's
   ion channels, while the capacitor models the insulating lipid membrane.
   Variable resistors are used for voltage-gated ion channels, as their
   resistance changes with voltage. A fixed resistor represents the
   potassium leak channels that maintain the membrane's resting potential.
   The sodium and potassium gradients across the membrane are modeled as
   voltage sources ( batteries).

Propagation

   Propagating action potentials can be modeled by joining several RC
   circuits, each one representing a patch of membrane.
   Enlarge
   Propagating action potentials can be modeled by joining several RC
   circuits, each one representing a patch of membrane.

   In unmyelinated axons, action potentials propagate as an interaction
   between passively spreading membrane depolarization and voltage-gated
   sodium channels. When one patch of cell membrane is depolarized enough
   to open its voltage-gated sodium channels, sodium ions enter the cell
   by facilitated diffusion. Once inside, positively-charged sodium ions
   "nudge" adjacent ions down the axon by electrostatic repulsion
   (analogous to the principle behind Newton's cradle) and attract
   negative ions away from the adjacent membrane. As a result, a wave of
   positivity moves down the axon without any individual ion moving very
   far. Once the adjacent patch of membrane is depolarized, the
   voltage-gated sodium channels in that patch open, regenerating the
   cycle. The process repeats itself down the length of the axon, with an
   action potential regenerated at each segment of membrane.

Speed of propagation

   Action potentials propagate faster in axons of larger diameter, other
   things being equal. They typically travel from 10-100 m/s. The main
   reason is that the axial resistance of the axon lumen is lower with
   larger diameters, because of an increase in the ratio of
   cross-sectional area to membrane surface area. As the membrane surface
   area is the chief factor impeding action potential propagation in an
   unmyelinated axon, increasing this ratio is a particularly effective
   way of increasing conduction speed.

   An extreme example of an animal using axon diameter to speed action
   potential conduction is found in the Atlantic squid. The squid giant
   axon controls the muscle contraction associated with the squid's
   predator escape response. This axon can be more than 1 mm in diameter,
   and is presumably an adaptation to allow very fast activation of the
   escape behaviour. The velocity of nerve impulses in these fibers is
   among the fastest in nature. Squids are notable examples of organisms
   with unmyelinated axons; the first tests to try to determine the
   mechanism by which impulses travel along axons, involving the detection
   of a potential difference between the inside and the surface of a
   neuron, were undertaken in the 1940s by Alan Hodgkin and Andrew Huxley
   using squid giant axons because of their relatively large axon
   diameter. Hodgkin and Huxley won their shares of the 1963 Nobel Prize
   in Physiology or Medicine for their work on the electrophysiology of
   nerve action potentials.

   In the autonomic nervous system in mammals, postganglionic neurons are
   unmyelinated. The small diameter of these axons (about 2 µ) results in
   a propagatory speed of approximately 1 m/s, as opposed to approximately
   18 m/s in myelinated nerve fibers of comparable diameter, thus
   highlighting the effect of myelination on the speed of transmission of
   impulses.

Saltatory conduction

   In myelinated axons, saltatory conduction is the process by which an
   action potential appears to jump along the length of an axon, being
   regenerated only at uninsulated segments (the nodes of Ranvier).
   Saltatory conduction increases nerve conduction velocity without having
   to dramatically increase axon diameter.

   Saltatory conduction has played an important role in the evolution of
   larger and more complex organisms whose nervous systems must rapidly
   transmit action potentials across greater distances. Without saltatory
   conduction, conduction velocity would need large increases in axon
   diameter, resulting in organisms with nervous systems too large for
   their bodies.

Detailed mechanism

   The main impediment to conduction speed in unmyelinated axons is
   membrane capacitance. In an electric circuit, the capacity of a
   capacitor can be decreased by decreasing the cross-sectional area of
   its plates, or by increasing the distance between plates. The nervous
   system uses myelin as its main strategy to decrease membrane
   capacitance. Myelin is an insulating sheath wrapped around axons by
   Schwann cells and oligodendrocytes, neuroglia that flatten their
   cytoplasm to form large sheets made up mostly of plasma membrane. These
   sheets wrap around the axon, moving the conducting plates (the intra-
   and extracellular fluid) farther apart to decrease membrane
   capacitance.

   The resulting insulation allows the rapid (essentially instantaneous)
   conduction of ions through a myelinated segment of axon, but prevents
   the regeneration of action potentials through those segments. Action
   potentials are only regenerated at the unmyelinated nodes of Ranvier
   which are spaced intermittently between myelinated segments. An
   abundance of voltage-gated sodium channels on these bare segments (up
   to four orders of magnitude greater than their density in unmyelinated
   axons ) allows action potentials to be efficiently regenerated at the
   nodes of Ranvier.

   As a result of myelination, the insulated portion of the axon behaves
   like a passive wire: it conducts action potentials rapidly because its
   membrane capacitance is low, and minimizes the degradation of action
   potentials because its membrane resistance is high. When this passively
   propagated signal reaches a node of Ranvier, it initiates an action
   potential, which subsequently travels passively to the next node where
   the cycle repeats.

Resilience to injury

   The length of myelinated segments of axon is important to saltatory
   conduction. They should be as long as possible to maximize the length
   of fast passive conduction, but not so long that the decay of the
   passive signal is too great to reach threshold at the next node of
   Ranvier. In reality, myelinated segments are long enough for the
   passively propagated signal to travel for at least two nodes while
   retaining enough amplitude to fire an action potential at the second or
   third node. Thus, the safety factor of saltatory conduction is high,
   allowing transmission to bypass nodes in case of injury.

Role in disease

   Some diseases degrade saltatory conduction and reduce the speed of
   action potential conductance. The most well-known of these diseases is
   multiple sclerosis, in which the breakdown of myelin impairs
   coordinated movement.

Refractory period

   Where membrane has undergone an action potential, a refractory period
   follows. Thus, although the passive transmission of action potentials
   across myelinated segments would suggest that action potentials
   propagate in either direction, most action potentials travel
   unidirectionally because the node behind the propagating action
   potential is refractory.

   This period arises primarily because of the voltage-dependent
   inactivation of sodium channels, as described by Hodgkin and Huxley in
   1952. In addition to the voltage-dependent opening of sodium channels,
   these channels are also inactivated in a voltage-dependent manner.
   Immediately after an action potential, during the absolute refractory
   period, virtually all sodium channels are inactivated and thus it is
   impossible to fire another action potential in that segment of
   membrane.

   With time, sodium channels are reactivated in a stochastic manner. As
   they become available, it becomes possible to fire an action potential,
   albeit one with a much higher threshold. This is the relative
   refractory period and together with the absolute refractory period,
   lasts approximately five milliseconds.

Evolutionary purpose

   The action potential, as a method of long-distance communication, fits
   a particular biological need seen most readily when considering the
   transmission of information along a nerve axon. To move a signal from
   one end of an axon to the other, nature must contend with physics
   similar to those that govern the movement of electrical signals along a
   wire. Due to the resistance and capacitance of a wire, signals tend to
   degrade as they travel along that wire over a distance. These
   properties, known collectively as cable properties set the physical
   limits over which signals can travel. Thus, nonspiking neurons (which
   carry signals without action potentials) tend to be small. Proper
   function of the body requires that signals be delivered from one end of
   an axon to the other without loss. An action potential does not so much
   propagate along an axon, as it is newly regenerated by the membrane
   voltage and current at each stretch of membrane along its path. In
   other words, the nerve membrane recreates the action potential at its
   full amplitude as it travels down the axon, thus overcoming the
   limitations imposed by cable physics.

Plant action potentials

   Many plants also exhibit action potentials that travel via their phloem
   to coordinate activity. The main difference between plant and animal
   action potentials is that plants primarily use potassium and calcium
   currents while animals typically use currents of potassium and sodium.

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