In physiology, an action potential occurs when the membrane potential of a specific axon location rapidly rises and falls: this depolarization then causes adjacent locations for the same depolarise. Potential action occurs in some types of animal cells, called exploitable cells, which include neurons, muscle cells, endocrine cells, and in some plant cells.
In neurons, action potential plays a central role in cell-to-cell communication by providing - or, with respect to salt conduction, aiding - propagating signals along the axons of neurons to the synaptic bunchons located at the end of the axon; these signals can then be connected to other neurons in synapses, or to motor cells or glands. In other cell types, the primary function is to activate the intracellular process. In muscle cells, for example, the action potential is the first step in the chain of events that causes contraction. In pancreatic beta cells, they provoke insulin release. The potential action in neurons is also known as " nerve impulse " or "nail", and the temporary sequence of action potential generated by neurons is called " rail spike ". A neuron that emits a potential action, or nerve impulse, is often said to be "fire".
The action potential is generated by a special type of voltage-gated ion channel that is embedded in the cell plasma membrane. These channels are closed when the membrane potential is close to the negative break potential of the cell, but they quickly begin to open if the membrane rises to a properly determined threshold voltage, depolarizing the transmembrane potential. When the channel is open, they allow the flow of sodium ions into, which converts the electrochemical gradient, which in turn results in a further increase in the membrane potential. This then causes more channels to open, generating greater electrical current across the cell membrane, and so on. The process takes place explosively until all available ion channels are open, resulting in a large increase in membrane potential. The rapid entry of sodium ions causes the polarity of the plasma membrane to reverse direction, and the ion channel then quickly becomes inactive. When the sodium channel closes, the sodium ions can no longer enter the neurons, and then they are actively transported out of the plasma membrane. The potassium channel is then activated, and there is a potassium ion outflow, returning the electrochemical gradient to a resting state. Once the potential action has occurred, there is a temporary negative shift, called afterhyperpolarization.
In animal cells, there are two main types of action potentials. One type is generated by a voltage-gated sodium channel, the other by a voltage-gated calcium channel. Sodium-based action potentials typically last for less than a millisecond, but calcium-based action potentials may last for 100 milliseconds or longer. In some types of neurons, slow calcium spikes provide a driving force for the long spikes of rapidly emitted sodium nails. In the heart muscle cells, on the other hand, the initial rapid sodium spike provides a "primer" to provoke the rapid start of a calcium spike, which then results in muscle contraction.
In the Hodgkin-Huxley membrane capacitance model, the transmission speed of the action potential is undefined and it is assumed that adjacent regions become depolarized due to ion disturbance being released with neighboring channels. Measurements of ion diffusion and radii have shown this to be impossible. In addition, contradictory measurements of entropy changes and timing of the capacitance model as acting alone.
Video Action potential
Ikhtisar
Nearly all cell membranes in animals, plants and fungi maintain a voltage difference between the exterior and the inside of the cell, called the membrane potential. The typical voltage across the animal cell membrane is -70 mV. This means that the interior of the cell has a negative voltage of about one-tenthenen volts relative to the exterior. In most cell types, the membrane potential usually remains fairly constant. Some cell types, however, are electrically active in the sense that their stress fluctuates over time. In some types of electrically active cells, including neurons and muscle cells, voltage fluctuations often take the form of rapid upward surge followed by rapid decline. This up-and-down cycle is known as the action potential . In some types of neurons, the entire up-and-down cycle lasts for a few thousandths of a second. In muscle cells, the typical action potential lasts about one fifth of a second. In some other types of cells, and also in plants, the potential action may last three seconds or more.
The electrical properties of a cell are determined by the structure of the membrane that surrounds it. The cell membrane consists of a lipid bundle of molecules in which larger protein molecules are embedded. The lipid bilayer is very resistant to the movement of electrically charged ions, thus functioning as an insulator. Proteins embedded in large membranes, by contrast, provide a channel through which the ions can pass through the membrane. The action potential is driven by a channel protein whose configuration switches between closed and open states as a function of the voltage difference between the interior and the exterior of the cell. This voltage sensitive protein is known as a voltage-gated ion channel.
Processing in a typical neuron
All cells in animal body tissues are electrically polarized - in other words, they maintain a voltage difference in the cell plasma membrane, known as the membrane potential. This electrical polarization results from the intricate interactions between the structure of proteins embedded in membranes called ion pumps and ion channels. In neurons, the type of ion channels in the membrane usually vary in different parts of the cell, providing dendrites, axons, and cell bodies of different electrical properties. As a result, some parts of the neuron membrane may be excited (capable of generating action potentials), while others are not. Recent research shows that the most excited part of the neuron is the part after the axon hillock (the point at which the axons leave the cell body), called the initial segment, but the axons and body cells are also vibrant in many cases..
Each advantageous patch of the membrane has two important membrane potential levels: the break potential, which is the membrane's potential value to maintain as long as nothing interferes with the cell, and a higher value is called the threshold potential. On a small hill axon of a typical neuron, the potential breaks about -70 millivolts (mV) and a potential threshold of about -55 mV. Synaptic input to neurons causes membranes to depolarize or hyperpolarization; that is, they cause the membrane potential to rise or fall. Potential action is triggered when enough depolarisation accumulates to bring the membrane potential up to the threshold. When the action potential is triggered, the potential of the membrane suddenly twists upward and then equally falls back down, often ending below the break level, where it remains for some period of time. The form of action potential is stereotypes; this means that ups and downs usually have roughly the same amplitude and time for all the action potentials in a given cell. (Exceptions are discussed later in the article). In most neurons, the whole process takes about a thousandth of a second. Many types of neurons emit the potential of action constantly at rates up to 10-100 per second. However, some types are much quieter, and may run for a few minutes or longer without radiating any potential action.
Maps Action potential
Basic biophysics
Potential action results from presence in special type cell membranes of voltage-gated ion channels. The voltage-gated ion channel is a group of proteins embedded in a membrane that has three key properties:
- This is capable of assuming more than one conformation.
- At least one conformation produces a channel through a penetrating membrane to a certain ionic type.
- The transition between conformations is affected by the membrane potential.
Thus, the voltage-gated ion channel tends to open for some membrane potential values, and is closed to the other. In many cases, however, the relationship between membrane potential and channel state is probabilistic and involves time delays. The ion channel switches between conformations at unpredictable times: The membrane potential determines the transition rate and the probability per time unit of each transition type.
The voltage-gated ion channel is capable of generating an action potential because they can generate a positive feedback loop: The membrane potential controls the state of the ion channel, but the ion channel state controls the membrane potential. Thus, in some situations, an increase in membrane potential may cause an open ion channel, thus causing a further increase in membrane potential. The potential action occurs when the positive feedback cycle is explosive. The time and trajectory of the amplitude of the action potential is determined by the biophysical nature of the voltage-gated ion channel which produces it. Some types of channels capable of generating the positive feedback needed to generate potential action do exist. The voltage-gated sodium channel is responsible for the rapid action potential involved in nerve conduction. Slower action potentials in muscle cells and some types of neurons are generated by the voltage-gated calcium channel. Each of these types comes in several variants, with different voltage sensitivities and different temporal dynamics.
The most-studied type of voltage-dependent ion channel consists of sodium channels involved in rapid nerve conduction. This is sometimes known as the Hodgkin-Huxley sodium channel because they were first characterized by Alan Hodgkin and Andrew Huxley in their Nobel Prize-winning research on the biophysics of action potential, but can be more easily referred to as Na > V channel. (The "V" means "voltage".) The channel Na V has three possible statuses, known as disabled , enabled , and is inactive . This channel can only be reset to sodium ions while in a state of enabled . When the membrane potential is low, the channel spends most of its time in a disabled (closed) state. If the membrane potential is raised above a certain level, the channel indicates the possibility of an increased transition to a state of enabled (open). The higher the membrane potential the greater the activation probability. Once the channel is activated, it will eventually transition to the inactivation (closed) state. This tends to then remain inactive for some time, but, if the membrane potential becomes lower again, the channel will eventually transition back to the disabled state. During the action potential, most of these types of channels through the cycle are disabled -> enabled -> inactive -> disabled disabling directly to country enabled is very low: Channels in country off are refractories until it has been redirected back to state disabled .
The result of all this is that the kinetics of the channels Na V are governed by a transition matrix whose tariffs depend on stress in a complex way. Since this channel itself plays a major role in determining stress, the global dynamics of the system can be very difficult to solve. Hodgkin and Huxley approached the problem by developing a set of differential equations for the parameters governing ion channel states, known as Hodgkin-Huxley equations. These equations have been extensively modified by subsequent research, but form the starting point for most theoretical studies of potential biophysical action.
As the membrane potential increases, the sodium ion channel opens, allowing the entry of sodium ions into the cell. This is followed by the opening of a potassium ion channel which allows the release of potassium ions from the cell. The inward flow of sodium ions increases the concentration of positively charged cations in the cell and causes depolarization, where the cell potential is higher than the cell rest potential. Sodium channels close at the peak of action potential, while potassium continues to leave the cell. The depletion of potassium ions decreases the membrane potential or cell hyperpolarizes. For a small voltage increase from the break, the potassium current exceeds the sodium current and the voltage returns to its normal resting value, typically -70 mV. However, if the voltage rises across the critical threshold, usually 15 mV higher than the resting value, the sodium current dominates. This results in a runaway condition in which positive feedback from sodium currently activates more sodium channels. Thus, cells light up , producing an action potential. The frequency at which neurons generate action potentials is often referred to as burn rate or nerve activation rate .
The current generated by the opening of the voltage-gated channel in the course of action potential is usually significantly greater than the initial stimulation currents. Thus, the amplitude, duration, and shape of the action potential are determined largely by the properties of the membrane being evaporated rather than the amplitude or duration of the stimulus. These all or none of the properties of the action potential distinguish it from assessed potentials such as potential receptors, electotonic potential, and synaptic potential, which are scaled by the size of the stimulus. Various types of action potential exist in many cell types and cell compartments as determined by the type of voltage-gated channel, leakage channel, channel distribution, ion concentration, membrane capacitance, temperature, and other factors.
The major ions involved in the action potential are sodium and potassium cation; the sodium ions enter the cell, and the potassium ion leaves, restoring the balance. Relatively few ions need to cross the membrane for membrane voltage to change drastically. Ions exchanged for action potential, therefore, make negligible changes in the ionic concentration of the interior and exterior. Some of the crossed ions are pumped again by the continuous action of the sodium-potassium pump, which, with other ion carriers, maintains the normal ratio of ion concentrations across the membrane. Calcium cations and chloride anions are involved in several types of action potentials, such as heart action potential and action potential in single cell algae Acetabularia , respectively.
Although the action potential is generated locally in the patch of a volatile membrane, the resulting current may trigger an action potential on adjacent neighboring membranes, accelerating propagation such as domino. In contrast to the passive dissemination of electrical potential (electotonic potential), the action potential is generated again along the membrane seepage and propagates without decay. The myelinated part of the axon is unexcited and produces no action potential and the signal is passively distributed as an electotonic potential. Spaces without regularly spaced myelinated spaces, called Ranvier nodes, generate an action potential to increase the signal. Known as salt conduction, this type of signal propagation provides a favorable tradeoff of signal speed and axon diameter. Depolarization of the axon terminal, in general, triggers the release of neurotransmitters into the synaptic cleft. In addition, the potential for backpropagating action has been noted in pyramidal neuron dendrites, which are ubiquitous in the neocortex. This is thought to have a role in spike-timing-dependent plasticity.
Electrical property maturation of the action potential
The ability of neurons to generate and disseminate potential action changes during development. How many membrane potentials of a neuron change as a result of current impulses is a function of membrane input resistance. As the cell grows, more channels are added to the membrane, causing a decrease in input resistance. An adult neuron also undergoes a shorter change in the membrane potential in response to the synaptic stream. The neurons of the lateral geniculate ferret muscle have longer time constants and greater voltage deflection at P0 than in P30. One consequence of the decreased duration of action potential is that the allegiance of the signal can be maintained in response to high-frequency stimulation. Immature neurons are more susceptible to synaptic depression than potentiation after high-frequency stimulation.
In the early development of many organisms, the action potential is actually initially carried by the calcium stream rather than the sodium stream. Kinetics of opening and closing the calcium channel during development are slower than the voltage-gated sodium channel which will carry action potentials in adult neurons. Longer opening times for calcium channels can lead to a much slower action potential compared to adult neurons. Xenopus neurons initially have a potential action that takes 60-90 ms. During development, this time is reduced to 1 ms. There are two reasons for this drastic decline. First, the inward flow becomes mainly carried by the sodium channel. Second, the delayed rectifier, the potassium channel current, increases to 3.5 times its initial strength.
In order for a transition from a calcium dependent action potential to a sodium dependent action potential to continue a new channel must be added to the membrane. If Xenopus neurons grow in environments with RNA synthesis or protein synthesis inhibitors, the transition is prevented. Even the electrical activity of the cell itself can play a role in channel expression. If the action potential in Xenopus myocytes is blocked, a typical increase in sodium and potassium density is prevented or delayed.
This maturation of electrical properties is seen throughout the species. Sodium Xenopus and potassium increase dramatically after neurons pass through the final phase of mitosis. The sodium flow density of cortical neurons of rats increased by 600% in the first two weeks postpartum.
Neurotransmission
Anatomy of neuron
Some types of cells support action potentials, such as plant cells, muscle cells, and specialized cells of the heart (where cardiac action potential occurs). However, the primary excitable cell is the neuron, which also has the simplest mechanism for action potential.
Neurons are electroactive cells consisting of, in general, of one or more dendrites, one soma, one axon and one or more axon terminals. Dendrites are cellular projection whose main function is to receive synaptic signals. Their protrusions, known as dendritic spines, are designed to capture the neurotransmitters released by presinaptic neurons. They have a high concentration of ligand-gated ion channels. This spine has a thin neck that connects the bulge to the dendrite round. This ensures that changes occurring within the spine tend to affect neighboring thorns. Dendritic spines can, with rare exceptions (see LTP), act as independent units. Dendrites extend from the soma, which shelters the nucleus, and many eukaryotic organelles are "normal". Unlike the thorns, the soma surface is filled by ion-activated voltage channels. This channel helps to transmit signals generated by dendrites. Appearing from soma is an axon hill. This region is characterized by having a very high concentration of voltage-activated sodium channels. In general, this is considered a zone of spike initiation for potential action, the trigger zone. Some of the signals generated in thorns, and transmitted by soma all blend here. As soon as the axon hill is an axon. This is a thin tubular bulge that moves away from the soma. This axon is isolated by the myelin sheath. Myelin consists of Schwann cells (in the peripheral nervous system) or oligodendrocytes (in the central nervous system), both of which are glial cell types. Although glial cells are not involved with the transmission of electrical signals, they communicate and provide important biochemical support for neurons. To be more specific, myelin wraps several times around the axonal segment, forming a thick layer of fat that prevents the ions from entering or leaving the axon. This isolation prevents significant signal decay and ensures faster signal speed. This isolation, however, has the limitation that no channel can be present on the axon surface. Therefore, there are regular membrane reservoirs, which have no isolation. These Ranvier knots can be regarded as "mini axon hillock", because the goal is to improve the signal to prevent significant signal decay. At the furthest end, the axon loses its insulation and begins to branch off into several axon terminals. This presinaptic terminal, or synaptic bunchons, is a special area within the axon of presinaptic cells containing neurotransmitters that are enclosed in small spheres called synaptic vesicles.
Initiation
Before considering the spread of action potential along the axon and its discontinuation on synaptic knobs, it is helpful to consider the methods in which the action potential can be initiated in axon hillock. The basic requirement is that the membrane voltage on a small hill is raised above the threshold for combustion. There are several ways in which this depolarization can occur.
Dynamics
The potential action is most often initiated by the excitatory postsynaptic potential of presinaptic neurons. Usually, neurotransmitter molecules are released by presinaptic neurons. The neurotransmitter then binds to the receptor on the postsinaptic cell. This binding opens up various types of ion channels. This opening has the effect of further altering the local permeability of the cell membrane and, thus, the membrane potential. If the binding increases the voltage (membrane depolarization), the synapse stimulates. However, if the binding reduces the voltage (hyperpolarizes membrane), it is inhibition. Whether the voltage increases or decreases, the change passes passively to the nearest area of ​​the membrane (as described by the cable equation and its perfection). Typically, the voltage stimulus decays exponentially with the distance from the synapses and with time from the neurotransmitter binding. Some fractions of excitatory stress can reach the axon hill and may (in rare cases) depolarize enough membranes to provoke new action potentials. More specifically, the stimulating potential of some synapses must work together at about the same time to provoke new potential action. Their mutual efforts can be thwarted, by inhibiting the potential for post-terminating inhibition.
Neurotransmission can also occur through electrical synapses. Due to the direct relationship between cells that expand in the form of a gap junction, an action potential can be transmitted directly from one cell to the next in both directions. The ion-free intercellular flow allows rapid, non-chemical-mediation transmission. Fixing the channel ensures that the action potential moves in only one direction through an electrical synapse. Electric synapses are found in all nervous systems, including the human brain, although they are a different minority.
Phase
The course of action potential can be divided into five parts: up phase, peak phase, fall phase, undershoot phase, and refractory period. During the rising phase, the membrane has the potential to depolarize (become more positive). The point at which depolarization stops is called the peak phase. At this stage, the membrane potential reaches the maximum. After this, there is a falling phase. During this stage the membrane potential becomes more negative, returning to the break potential. The undershoot, or afterhyperpolarization, phase is the period in which the temporary membrane potential becomes more negatively charged than at rest (hyperpolarized). Finally, the time at which the next potential action is impossible or difficult to burn is called the refractory period, which may overlap with other phases.
The course of action potential is determined by two combined effects. First, the voltage-sensitive ion channels open and close in response to changes in the membrane voltage V m . This changes the membrane permeability to the ions. Second, according to the Goldman equation, this change in permeability changes the equilibrium potential of E m , and, thus, the membrane voltage V m . Thus, the membrane potential affects the permeability, which then affects the membrane potential. This forms the possibility for positive feedback, which is an important part of the rising phase of the action potential. A troubling factor is that an ion channel may have several internal "gates" that respond to changes in V <> m in the opposite way, or at different levels. For example, although it raises V m opens most of the gates in the voltage-sensitive sodium channel, it also closes the channel gate inactivation ", albeit more slowly. Therefore, when V m is raised suddenly, the sodium channel opens initially, but is then closed due to slower inactivation.
The voltage and current potential of action at all phases were accurately modeled by Alan Lloyd Hodgkin and Andrew Huxley in 1952, where they were awarded the Nobel Prize in Physiology or Medicine in 1963. However, their model only considered two types of voltage-sensitive ion channels, and make some assumptions about them, for example, that their internal gates open and close independently of each other. In fact, there are many types of ion channels, and they do not always open and close independently.
Stimulation and up phase
The typical action potential starts at axon hillock with a strong enough depolarization, for example, a stimulus that increases V <> m . This depolarization is often caused by the injection of extra sodium cations into cells; These cations may come from various sources, such as chemical synapses, sensory neurons or potential pacemakers.
For neurons at rest, there is a high concentration of sodium and chloride ions in the extracellular fluid compared to the intracellular fluid while there is a high concentration of potassium ions in the intracellular fluid compared to the extracellular fluid. This concentration gradient along with a potassium leakage channel present on the neuron membrane leads to the depletion of potassium ions making a potential break close to E K Ã,? -75 mV. Depolarization opens both the sodium and potassium channels in the membrane, allowing the ions to flow in and out of the axons, respectively. If a small depolarization (eg, increases V m from -70 mV to -60 mV), the outer potassium currents will flood the sodium stream inward and the membrane is polarized back to normal resting potential about -70 mV. However, if the depolarization is large enough, the sodium current in increased over the potassium current and the escape conditions (positive feedback) results: the more inward flow, the more V m increases , which in turn further increases the inward flow. A fairly strong depolarization (increased V <> m ) causes a voltage-sensitive sodium channel to open; increased permeability to sodium drive V m closer to the equilibrium voltage of sodium E Na ? 55 mV. Increased voltage in turn causes more sodium channels to open, which pushes V <> m further farther towards E Na . This positive feedback continues until the open sodium channel is full and V m is close to E Na . The sharp rise in V m and sodium permeability corresponds to the rising phase of the action potential.
The critical threshold voltage for this runaway condition is usually around -45 mV, but it depends on recent axon activity. The membrane that just issued the action potential can not directly fire the other, because the ion channel has not returned to the disabled state. The period in which no new action potential can be fired is called absolute refractory period . At a later time, after some but not all ion channels have recovered, axons can be stimulated to produce other action potentials, but with a higher threshold, requiring a stronger depolarization, for example, up to -30 mV. The period when the extraordinary action potential is difficult to generate is called relative refractory period .
Peak and fall phase
Positive feedback from the rising phase slows and stops when the sodium ion channel becomes fully open. At the peak of the action potential, the permeability of sodium is maximized and the membrane voltage V m is almost equal to the sodium equilibrium voltage E Na . However, the same voltage increase that opens the sodium channel initially also gently closes it, by closing their pores; sodium channels become inactive . This lowers the membrane permeability of sodium relative to potassium, pushing the membrane voltage back to the resting value. At the same time, the rising voltage opens the potassium voltage-sensitive channel; increased potassium permeability of the drive membrane V m to E K . Combined, changes in sodium and potassium permeability cause V <> m to drop rapidly, membrane repolarization and produce a "falling phase" of the action potential.
Afterhyperpolarization
The raised voltage opens more potassium channels than usual, and some do not close immediately when the membrane returns to its normal resting voltage. In addition, the potassium channel is further exposed in response to the inclusion of calcium ions during the action potential. The membrane potassium permeability is unusually high, pushing the membrane voltage V m even closer to the potassium equilibrium E K . Therefore, there is undershoot or hyperpolarization, called afterhyperpolarization in technical language, which persists until the permeability of the membrane potassium returns to its usual value.
Refractory period
Each action potential is followed by a refractory period, which can be divided into absolute refractory period , where it is impossible to generate other action potentials, and then relative refractory periods >, where stronger stimuli are needed than usual. These two refractory periods are due to changes in molecular state of sodium and potassium channels. When closing after the action potential, the sodium channel enters the "inactive" state, where they can not be made to open regardless of the membrane potential - this gives rise to an absolute refractory period. Even after sufficient amounts of sodium channels have been diverted back to their resting state, it is often the case that a small portion of the potassium channel remains open, making it difficult for the membrane to depolarize potential, thus creating a relative refractory period. Because the density and subtypes of potassium can vary greatly between different types of neurons, the duration of the refractory period is relatively variable.
The absolute refractory period is largely responsible for the propagation of the direction of potential action along the axon. At any given moment, the axon patches behind the refractory spiking part are active, but the patch up front, has not been activated recently, is capable of being stimulated by depolarization of the action potential.
Propagation
The potential action generated in the axon hole spreads as a wave along the axon. The current that flows inward at the point in the axon as long as the action potential spreads along the axon, and depolarizes the adjacent part of the membrane. If strong enough, this depolarization provokes the same potential action in the neighboring membrane patch. This basic mechanism was demonstrated by Alan Lloyd Hodgkin in 1937. After destroying or cooling the nerve segment and thereby blocking the potential for action, he indicated that potential action arrive on one side of the block could provoke another potential action on the other, provided that the segment is blocked enough short.
Once the potential action has occurred on a membrane patch, the membrane patch takes time to recover before it can shoot again. At the molecular level, this absolute refractory period corresponds to the time required for a voltage activated sodium channel to recover from inactivation, that is, to return to its closed state. There are many types of potassium channels that are activated with the voltage in the neuron. Some of them disable fast (A-type currents) and some of them disable slowly or not disable altogether; this variability ensures that there will always be a source of current available for repolarization, even if some potassium channels are inactive due to prior depolarization. On the other hand, all sodium channels activated disabling neural voltages within a few milliseconds during strong depolarization, thus making the following depolarization unlikely until most of the sodium channels have returned to a closed state. Although limiting the firing frequency, the absolute refractory period ensures that the action potential moves only one direction along the axon. The current flows in because the action potential spreads in both directions along the axon. However, only the unused portion of the axon may respond with potential action; the part that has just been fired is unresponsive to the potential for safe action beyond reach and can not estimate that part. In ordinary orthodromic conduction, the action potential diffuses from the axon hill toward the synaptic button (termini axon); propagation in the opposite direction - known as antidromic conduction - is very rare. However, if the laboratory axon is stimulated in the middle, the two parts of the axon are "fresh", that is, not wired; then two action potentials will be generated, one trip to the axon hill and the other moving toward the synaptic keys.
Myelin and salt conduction
To allow for rapid and efficient electrical signal transduction in the nervous system, certain neural axons are covered with myelin sheaths. Myelin is a multilamellar membrane that encloses axons in segments separated by intervals known as Ranvier nodes. It is produced by special cells: Schwann cells exclusively in the peripheral nervous system, and oligodendrocytes exclusively in the central nervous system. The myelin sheath reduces the membrane capacitance and increases the membrane resistance in the inter-node interval, thus allowing rapid and steamy action potential action from node to node. Mielinations are found mainly in vertebrates, but analog systems have been found in several invertebrates, such as some species of shrimp. Not all neurons in vertebrates have myelin; for example, the axons of neurons consisting of autonomic nervous systems are not, in general, myelinated.
Myelin prevents ions from entering or leaving axons along the myelin segment. As a general rule, myelination increases the speed of conduction of action potential and makes it more energy efficient. Whether salt or not, the average conduction velocity of the action potential ranges from 1 meter per second (m/s) to over 100 m/s, and, in general, increases with axonal diameter.
The potential action can not be spread through the membrane in the myelinated segment of the axon. However, the current is carried by the cytoplasm, which is sufficient to depolarize the first or second subsequent Ranvier node. Conversely, the ion current from the action potential on a Ranvier node provokes another potential action action at the next node; this obviously "jumps" from the action potential from node to node known as salt conduction. Although the salt conduction mechanism was suggested in 1925 by Ralph Lillie, the first experimental evidence for salt conduction came from Ichiji Tasaki and Taiji Takeuchi and from Andrew Huxley and Robert StÃÆ'¤mpfli. In contrast, in unmyelinated axons, the potential of action provokes the other in the direct bordering membrane, and moves steadily down the axon like a wave.
Myelin has two important advantages: fast conduction velocity and energy efficiency. For axons greater than the minimum diameter (approximately 1 micrometer), the mielination increases the conduction velocity of the action potential, typically tenfold. In contrast, for the given conduction velocity, the mielin fibers are smaller than those of the nonelilin counterparts. For example, the action potential travels at approximately the same speed (25 m/sec) in a myelinated katon axon and a giant squid axon without myelinated, but the axon frog has a diameter of about 30-fold smaller and 1000-fold smaller cross-sectional area.. Also, since ion currents are confined to Ranvier nodes, much less ion "leaks" across the membrane, saving metabolic energy. This savings is a significant selective advantage, because the human nervous system uses about 20% of the body's metabolic energy.
The length of the myelinated axon segment is important for the success of saltatory conduction. They should be as long as possible to maximize the speed of conduction, but not so long that the coming signal is too weak to lure the action potential at the next Ranvier node. In nature, myelinated segments are generally long enough for passive propagation signals to travel for at least two nodes while retaining sufficient amplitude to fire the action potential at the second or third node. Thus, the salt conduction safety factor is high, allowing transmission to cut the knot in case of injury. However, the potential for action may end prematurely in certain places where safety factors are low, even in nonmelelin neurons; a common example is the branch point of the axon, where it is divided into two axons.
Some diseases lower myelin and damage salt conduction, reducing the conduction velocity of action potential. The most notable are multiple sclerosis, in which myelin disorders impair coordinated movements.
Cable Theory
The current flow in axon can be explained quantitatively by cable theory and elaboration, such as the compartment model. The cable theory was developed in 1855 by Lord Kelvin to model transatlantic telegraph cables and proved relevant to neurons by Hodgkin and Rushton in 1946. In simple cable theory, neurons are treated as electrical passive electrical and passive electric cables. can be described by a partial differential equation
where V ( x , t ) is the voltage across the membrane at a time t along the neurons, and where? and? is a long scale and characteristic time where the voltage declines in response to the stimulus. Referring to the circuit diagram on the right, this scale can be determined from resistance and capacitance per unit length.
This time and scale can be used to understand the dependence of the conduction velocity on the diameter of the neuron in the nonelelin fibers. For example, the time scale? increases with both membrane resistance r m and capacitance c m . As the capacitance increases, more charge must be transferred to produce the transmembrane voltage given (with the equation Q Ã, = Ã, CV ); as the resistance increases, the less cost is transferred per unit time, making equilibrium slower. In the same way, if the internal resistance per unit length r i is lower in one axon than the other (for example, since the former radius is larger), the length of spatial decay ? becomes longer and the conduction velocity of an action potential must increase. If transmembrane resistance r m increases, which decreases the mean "leakage" current across the membrane, also causing ? becomes longer, increasing the speed of conduction.
Termination
Chemical synapses
In general, the action potential that reaches the synaptic buttons causes the neurotransmitter to be released into the synaptic cleft. Neurotransmitters are small molecules that can open ion channels in postsynaptic cells; most axons have the same neurotransmitters on all of their termini. The arrival of the action potential opens the voltage sensitive calcium channel in the presinaptic membrane; the inclusion of calcium causes the vesicles to be filled with neurotransmitters to migrate to the cell surface and release their contents into the synaptic cleft. This complex process is inhibited by neurotoxins tetanospasmin and botulinum toxin, which are responsible for tetanus and botulism, respectively.
Electrical synapses
Some synapses remove the "intermediate" from the neurotransmitter, and connect the presinaptic and postcapsinetic cells together. When an action potential reaches the synapse, the ion current flowing into the presinaptic cell can cross the barrier of the two cell membranes and enter the postsinaps cell through the pores known as the connexons. Thus, the ion currents of the precinitic action potential can directly stimulate the postinaptic cell. Electric synapses allow for faster transmission because they do not require the slow diffusion of neurotransmitters in the synaptic cleft. Therefore, electrical synapses are used whenever fast response and time coordination are essential, such as in reflex escape, vertebrate retina, and heart.
Neuromuscular joint
A special case of chemical synapses is a neuromuscular junction, in which the motor neuron axons end in the muscle fibers. In such cases, the released neurotransmitter is acetylcholine, which binds to acetylcholine receptors, integral membrane proteins in the membrane ( sarcolemma ) of the muscle fibers. However, acetylcholine does not remain bonded; instead, it dissociates and is hydrolyzed by the enzyme, acetylcholinesterase, located in the synapse. This enzyme quickly reduces the stimulus to the muscles, allowing the degree and timing of muscle contractions to be carefully regulated. Some toxins inactivate acetylcholinesterase to prevent this control, such as sarin and tabun, and diazinon and malathion insecticides.
Other cell types
Potential heart action
The potential action of the heart differs from the nerve action potential by having an extended plateau, where the membrane is held at high stress for several hundred milliseconds before being released by the potassium current as usual. The plateau is caused by the slower channel action of calcium opening and holding the membrane voltage near their equilibrium potential even after the sodium duct is off.
The potential for cardiac action plays an important role in coordinating the contraction of the heart. The heart cells of the sinoatrial node provide the potential for a heart pacemaker that aligns the heart. The potential action of these cells spreads to and through the atrioventricular node (AV node), which is usually the only conduction path between the atria and the ventricles. The action potential of the AV node moves through his bundle and from there to Purkinje fibers. Conversely, anomalies in heart action potential - whether due to congenital mutations or injury - can lead to human pathology, especially arrhythmias. Some anti-arrhythmia drugs act on the potential action of the heart, such as quinidine, lidocaine, beta blockers, and verapamil.
Potential muscle action
The potential action in normal skeletal muscle cells is similar to the action potential in neurons. The action potential is generated from the depolarization of the cell membrane (sarcolemma), which opens the sodium voltage sensitive channel; this becomes inactive and the membrane is released through the outflow of potassium ions. The potential break before the action potential is usually -90mV, is somewhat more negative than typical neurons. The potential for muscle action lasts about 2-4 ms., An absolute refractory period of about 1-3 ms, and a muscle conduction velocity of about 5 m/s. The action potential releases calcium ions that liberate the tropomyosin and allow the muscles to contract. The potential for muscle action is triggered by the arrival of pre-synaptic neuronal potential action at the neuromuscular junction, which is a common target for neurotoxins.
Plant action potential
Plant cells and fungi are also electrically excited. The fundamental difference for the potential action of animals is that depolarization in plant cells is not achieved by the uptake of positive sodium ions, but with the release of negative ions of chloride . Together with the following potassium ion release, which is common to plant and animal potentials, the action potential in plants means the loss of osmotic salts (KCl), whereas the osmotic action potential of animals is neutral, when equal amounts of sodium enter and leave potassium cancel each other osmotic. The interaction of electrical and osmotic connections in plant cells shows the osmotic function of electrical stimulation in common ancestors, plants and animals under changing conditions of salinity, while the current function of fast signal transmission is seen as a younger achievement of metazoan cells in the environment more stable osmotic. It should be assumed that the familiar action potential signaling functions in some vascular plants (eg Mimosa pudica ) appear independently of those in metazoan excited cells.
Distribution of taxonomy and evolutionary advantages
Action potentials are found throughout multicellular organisms, including plants, insect-like invertebrates, and vertebrates such as reptiles and mammals. Sponges appear to be the main phylum of multicellular eukaryotes that do not emit potential action, although some studies show that these organisms have a form of electrical signal as well. The break potential, as well as the size and duration of action potential, has not changed much with evolution, although the conduction velocity varies dramatically with axonal diameter and mielination.
Given its preservation throughout evolution, the potential for action seems to give an evolutionary advantage. One of the action potential functions is the rapid remote signaling within the organism; the conduction velocity can exceed 110 m/s, which is one-third the speed of sound. By comparison, the hormone molecules carried in the bloodstream move about 8 m/s in a large artery. Part of this function is the tight coordination of mechanical events, such as heart contractions. The second function is the calculation associated with its generation. Being an all-or-nothing signal that does not rot with the transmission distance, the action potential has advantages similar to that of digital electronics. The integration of various dendritic signals in axon hillocks and their thresholding to form the complex train of action potential is another form of computation, which has been biologically exploited to form a central pattern generator and emulated in artificial neural networks.
Experimental method
The study of potential action has required the development of new experimental methods. The initial work, prior to 1955, was undertaken primarily by Alan Lloyd Hodgkin and Andrew Fielding Huxley, who, along with John Carew Eccles, was awarded the 1963 Nobel Prize in Physiology or Medicine for their contribution to the basic description of ionic nerve conduction. It focuses on three purposes: isolating signals from a single neuron or axon, developing fast, sensitive electronics, and shrinking enough electrodes that the voltage inside a single cell can be recorded.
The first problem solved by studying the giant axons found in squid neurons ( Loligo forbesii and Doryteuthis pealeii , at that time was classified as Loligo pealeii i>). These axons are very large in diameter (about 1 mm, or 100 times larger than typical neurons) so that the axis is visible to the naked eye, making it easy to extract and manipulate. However, they do not represent all the vibrant cells, and many other systems with potential action have been studied.
The second problem is discussed with the important development of voltage clamp, which allows researchers to study the ion currents underlying the action potential in isolation, and eliminating the main source of electronic interference, current sub related to the capacitance of C of the membrane. Since the current is equal to C times the transmembrane voltage change rate V m , the solution is to design a circuit that stores V m fixed (zero rate change) regardless of the current flowing across the membrane. Thus, the current required to keep V m at a fixed value is a direct reflection of the current flowing through the membrane. Other electronic advancements include the use of Faraday enclosure and electronics with high input impedance, so the measurement itself does not affect the voltage being measured.
A third problem, that getting the electrode small enough to record the voltage in a single axon without interruption, was solved in 1949 by the invention of a glass micropipette electrode, which was quickly adopted by other researchers. Improvement of this method is capable of generating tips electrode as smooth as 100 ÃÆ'... (10 nm), which also confer high input impedance. The action potential can also be recorded with small metal electrodes placed directly next to neurons, with neurochips containing EOSFET, or optically with a dye sensitive to Ca 2 or to a voltage.
While the glass micropipette electrode measures the amount of current passing through many ion channels, studying the electrical properties of an ion channel became possible in 1970 with the development of a patch clamp by Erwin Neher and Bert Sakmann. For this discovery, they were awarded the Nobel Prize in Physiology or Medicine in 1991. Patch-clamping verifies that ionic channels have discrete conductance states, such as open, closed and inactive.
Optical imaging technologies have been developed in recent years to measure potential action, either through simultaneous multisite recording or with ultra-spatial resolution. By using a voltage-sensitive dye, the action potential has been optically recorded from a small patch of cardiomyocyte membrane.
Neurotoxins
Some neurotoxins, both natural and synthetic, are designed to block potential action. Tetrodotoxin from bloated fish and saxitoxin from Gonyaulax (genus dinoflagellata responsible for "red tides") blocks the action potential by inhibiting the voltage-sensitive sodium channel; likewise, dendrotoxin from the black mamba snake inhibits potassium-voltage-sensitive channels. Such ion channel inhibitors serve as important research objectives, allowing scientists to "turn off" certain channels at will, thus isolating the contribution of other channels; they can also be useful in purifying ion channels with affinity chromatography or in testing their concentration. However, the inhibitor also makes an effective neurotoxin, and has been considered for use as a chemical weapon. Neurotoxins directed at insect ion channels are effective insecticides; one example is the synthetic permethrin, which extends the activation of the sodium channels involved in the action potential. Insect ion channels are quite different from their human counterparts that there are some side effects in humans.
History
The electrical role in the nervous system of animals was first observed in the frogs dissected by Luigi Galvani, who studied them from 1791 to 1797. Galvani's results stimulated Alessandro Volta to develop the earliest Voltaic stacks - by which he studied animal electricity (such as electric eels) and physiological response to the applied direct current voltage.
The scientists of the 19th century studied the propagation of electrical signals across the nerves (ie, neuron bundles) and showed that the neural network consists of cells, not the interconnected tissue of the tube (a reticulum ). Carlo Matteucci follows up on the Galvani study and shows that the cell membrane has a voltage across it and can produce direct current. Matteucci's work inspired the German physiologist, Emil du Bois-Reymond, who discovered the potential for action in 1843. The potential action potential velocity was first measured in 1850 by du Bois-Reymond friend Hermann von Helmholtz. To establish that the neural network consists of discrete cells, Spanish physician Santiago RamÃÆ'³n y Cajal and his students use stains developed by Camillo Golgi to express the various forms of neurons, which they provide with great difficulty. For their discovery, Golgi and RamÃÆ'³n y Cajal were awarded the 1906 Nobel Prize in Physiology. Their work solved the long-standing controversy in the nineteenth century neuroanatomy; Golgi himself has debated the network model of the nervous system.
The 20th century was a significant era for electrophysiology. In 1902 and again in 1912, Julius Bernstein proposed the hypothesis that the action potential resulted from a change in the permeability of the axonal membrane into ions. The Bernstein hypothesis is confirmed by Ken Cole and Howard Curtis, which suggests that membrane conductance increases during action potential. In 1907, Louis Lapicque suggested that the potential action is generated as a crossed threshold, what would then be shown as a product of the dynamic system of ionic behavior. In 1949, Alan Hodgkin and Bernard Katz refined Bernstein's hypothesis considering that axonal membranes may have different permeabilities for different ions; in particular, they show an important role of sodium permeability for action potentials. Mere
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