Action potential
Under action potential ( AP short - even electrical excitation) is defined as a temporary, characteristic deviation of the membrane potential of a biological cell from its resting potential. For the course of a typical APs include: electrical inducibility with threshold potential, refractory period, Nachhyperpolarisation and propagation. The molecular mechanism of an AP is the interaction of voltage-sensitive ion channels. Especially good action potentials in the axon of nerve cells are examined. There they cause rapid conduction over long distances. This APe are the main subject of this article. Similar action potentials cause muscle contraction. Action potentials but also come in single-celled organisms (eg Paramecium and diatoms ) in algae (eg Chara spp ) and vascular plants (eg Mimosa ) ago.
An AP may take from about one millisecond (in the nerves) to several minutes (in some algae). An AP is a singular event with binary character. So there is no strong or weak action potentials, but there are all-or -nothing responses. They occur typically (but not exclusively) at the axon hillock of a nerve cell and migrate along the axon. The signal strength, often in response to a stimulus intensity is represented in the frequency of action potentials.
Alan Lloyd Hodgkin in 1952 laid and Andrew Fielding Huxley before a mathematical model that explains the origin of the action potential in the giant axon of the squid by the interplay of various ion channels and became famous under the name of Hodgkin -Huxley model. For this discovery, the two researchers got together with John Eccles 1963 Nobel Prize for Medicine.
AP spread along the cell body and dendrites and backward. The exact function of these backward forwarding is still under investigation. Axonal propagation from the cell body to Endknöpfchen is also (correctly) called orthodromically and antidromically opposite forwarding.
Cytological Basics
The causes of the formation and the particular properties of an action potential in the properties are of different groups of ion channels in the plasma membrane of the cell. An initial stimulus activated when it reaches a certain level (approximately -50 mV, the so-called threshold potential ), and regardless of how far he exceeds a chain of opening and closing operations of the channels which allow an ionic current, and thus change the membrane potential. The shape of the action potential is then independent of the strength of the trigger -threshold stimulus always uniform. This change in potential can bring in the next place the membrane again an electrical excitation, which is the basis of the excitation line.
Description of the potential curve
Starting from the resting membrane potential, which, depending on the cell type from -90 to -70 mV in neurons, are four phases of the action potential:
An action potential lasts about 1-2 ms in neurons, but can also cover a few hundred milliseconds ( in the heart ) extend.
Already during the repolarization is the cell in the refractory period. During this phase, first no ( absolute refractory period, about 0.5 ms ) and then only with increased stimulus ( increased threshold potential within the relative refractory period, about 3.5 ms), another action potential can be generated.
Causes of action potential
The explanation requires an understanding of the presented in the article to the resting membrane potential emergence of a resting membrane potential. Briefly, the following factors for the resting membrane potential are responsible:
- Chemical and electrical gradients of ions
- Selective permeability of ion channels
- Ion pump - in particular sodium-potassium pump.
Properties of the ion channels
As described in the item on the resting membrane potential, cells have a number of ion channels. Especially for certain specific sodium or potassium ions, ion channels are responsible for the animal action potential. These channels open as a function of membrane potential, i.e., they are voltage- activated. At rest, the membrane potential is negative.
Thus, a voltage-dependent sodium channel, for example, ( Nav - channel) ( because of its ability also referred to as a fast sodium channel) closed at resting membrane potential and activated. Upon depolarization, a channel-specific value of a conformational change takes place. The channel becomes permeable to ions and changes to the state on open. However, the channel does not remain open despite continued depolarization, but will be closed independently within a few milliseconds on the membrane potential again. This usually happens by a reason in the cytoplasm part of the channel protein, the inactivation domain, which is equal to a " plug " is located in the channel and clogs. This condition is referred to as closed and inactivated. The transition into the closed and activated only after a hyperpolarization ( or complete repolarization in heart muscle cells ) is possible, the transition from the closed state to the inactivated state and open is not possible in the simplified model.
The literature also describes that a closed and inactivated channel is initially present after repolarization briefly in the open state before he goes through the conformational change directly after closed activated. In any case, the re- activation occurs only after a hyperpolarization ( or complete repolarization in heart muscle cells), a transition inactivated after open is not possible at depolarized membrane.
Not all channels open simultaneously at the same value of the membrane potential. Rather, the probability of a channel to transition to a certain state depending on the voltage. From a purely statistical distribution of an equilibrium sets in, so that a larger number of channels in the sum very well fulfilled the above- described model.
Also, the time required to pass from one state to the other, channel-specific. In the described sodium channel conformational runs from closed to open in less than a millisecond, while a potassium channel requires time on the order of 10 ms.
Apart from the voltage, there are a number of other, often chemical factors for opening or closing the channels. Of which are for the action potential only two of certain (see below) meaning. Firstly, the inwardly rectifying potassium channels ( Kir ) are not regulated as such. However, there are low molecular weight, positively charged materials such as spermine, which may clog the channel pores with sufficient depolarization ( channel block, block the pores ). Another mechanism relates to potassium channels, which open when intracellular calcium ions (usually in very low concentration intracellular) bind to it.
The end of the action potential
Starting position
In the initial position the cell is at rest and has her resting membrane potential. The sodium channels are almost all closed, only certain potassium channels are open, the potassium ions determine the resting membrane potential. For all ion movement direction and strength by the electrochemical driving forces for the respective ions is determined. Especially sodium ions flow rapidly into the cell as soon as the channels open for it.
Initiation phase
During the initiation phase must by a stimulus, the membrane potential increase until the depolarization reaches a certain threshold. This can be through the opening of postsynaptic ion channels (Na , Ca2 ) or done by a elektrotonisch forwarded (action ) potential from an adjacent membrane region.
Increases the membrane potential by 20 mV ( for example, from -70 to -50 mV), the pore block of Kir channels occurs by spermine, which allows the subsequent very rapid depolarization and reaching the threshold of sodium channels, which otherwise by outflowing potassium ions, would act in the direction of the resting potential, would at least reduced.
Spreads and Over Shoot
At -60 mV, the voltage-dependent sodium channels NaV begin to transition to the open state. Sodium ions are removed with their high external concentration far from their electrochemical equilibrium, a flow, the cell depolarizes, be more voltage sensitive channels open; more ions to stream: The rapid spread leads to overshoot ( repolarization ). The " explosive " depolarization after exceeding the threshold value is based on positive feedback.
Beginning of the repolarization
Even before the potential maximum is reached, start the NaV channels to inactivate. At the same time the voltage-gated potassium channels KV come into play; K ions flow out of the cell. Although they have their threshold at similar values , but need much longer for the opening, which they are now starting slowly. During the peak of the Na - conductance potassium channels are currently open halfway, and reach their maximum when almost all Na channels are already inactivated. Characterized the Na maximum is a little before the voltage maximum, during the K maximum falls in the phase of the steepest repolarization.
Repolarization
During the repolarization potential approaches back to the resting potential. The KV close the pores block the Kir is canceled, which is important for the stabilization of the resting potential. The NaV channels are activated slowly.
Nachhyperpolarisation
In many cells (especially neurons ) is still observed hyperpolarization. It can be explained by a still more increased potassium conductance, thereby reducing the potential is even closer to the potassium equilibrium potential. The conductivity is higher because open corresponding potassium channels during the action potential inflowing calcium ions and normalized only when the calcium level drops again. Also an increased pumping rate of the sodium-potassium pump can contribute to the hyperpolarization.
Refractory
After the decay of the action potential the axon for a short time is not excited. The Arbeitsmyokardzellen of the heart, this phase is - also known there as " plateau phase " - particularly long, which is attributed to the so-called "slow calcium influx ." ( This fact is important in order to prevent a " running back " of the excitation ( unidirectionality ) ). This duration, the refractory period is determined by the time required for the re- activation of NaV. During the absolute refractory period shortly after the overshoot when the repolarization is still in progress, these channels can not reopen it. It also says the threshold is infinity. During the relative refractory period is required stronger stimuli and receives weaker action potentials. Here, the threshold of infinity moves again to its normal value.
Threshold potential
Most exceeding a certain threshold potential is blamed for triggering an action potential, from which the sodium channels are activated snowballed in the manner of an internal comparison. Despite all efforts to find such a firing threshold, no fixed voltage value can be specified, the conditional action potential. Instead, neurons fire under a relatively broad band of inducing membrane stresses. Therefore, the neuroscience has strayed from the notion of a fixed threshold potential. System Theoretically, the formation of the action potential best be described by a bifurcation between passive and action potential dynamics, as it is for example in the Hodgkin -Huxley model of the case. Nevertheless, it is also in the technical literature, quite common to continue to speak of a fire threshold to identify the gray area between resting and action potential.
Special animal action potentials
Except through voltage-activated sodium channels in Purkinje cells action potentials can be modulated in frequency by voltage-activated calcium channels.
Vegetable action potentials
In principle cells of plants and fungi are also electrically excitable. The main difference to animal action potential is that the depolarization is not by entry of positive sodium ions, but by discharge of negative chloride ions. Together with the subsequent discharge of positive potassium ions, which causes both in animal and in plant cells, repolarization, this means for plant cells an osmotic loss of potassium chloride, whereas the animal action potential is osmotically neutral by equal amounts of sodium influx and potassium efflux in total. The coupling of electrical and osmotic events during plant action potential suggests that electrical excitability in the common unicellular ancestor of animal and plant cells in regulating the salt budget served under varying salinity, while the osmotically neutral transmission of signals one by animal multicellular organisms with nearly constant salinity is evolutionarily younger achievement. Accordingly, the signaling function of action potentials in some vascular plants has ( Mimosa pudica example ) evolved independently from that in animal cells.