Action potential


If Xenopus neurons are grown in an environment with RNA synthesis or protein synthesis inhibitors that transition is prevented. The large membrane-embedded proteins, in contrast, provide channels through which ions can pass across the membrane.

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As a result, some parts of the membrane of a neuron may be excitable capable of generating action potentials , whereas others are not. Recent studies [ citation needed ] have shown that the most excitable part of a neuron is the part after the axon hillock the point where the axon leaves the cell body , which is called the initial segment, but the axon and cell body are also excitable in most cases.

Each excitable patch of membrane has two important levels of membrane potential: At the axon hillock of a typical neuron, the resting potential is around —70 millivolts mV and the threshold potential is around —55 mV. Synaptic inputs to a neuron cause the membrane to depolarize or hyperpolarize ; that is, they cause the membrane potential to rise or fall.

Action potentials are triggered when enough depolarization accumulates to bring the membrane potential up to threshold. When an action potential is triggered, the membrane potential abruptly shoots upward and then equally abruptly shoots back downward, often ending below the resting level, where it remains for some period of time.

The shape of the action potential is stereotyped; this means that the rise and fall usually have approximately the same amplitude and time course for all action potentials in a given cell. Exceptions are discussed later in the article. In most neurons, the entire process takes place in about a thousandth of a second. Many types of neurons emit action potentials constantly at rates of up to 10— per second. However, some types are much quieter, and may go for minutes or longer without emitting any action potentials.

Action potentials result from the presence in a cell's membrane of special types of voltage-gated ion channels. Thus, a voltage-gated ion channel tends to be open for some values of the membrane potential, and closed for others.

In most cases, however, the relationship between membrane potential and channel state is probabilistic and involves a time delay. Ion channels switch between conformations at unpredictable times: The membrane potential determines the rate of transitions and the probability per unit time of each type of transition.

Voltage-gated ion channels are capable of producing action potentials because they can give rise to positive feedback loops: The membrane potential controls the state of the ion channels, but the state of the ion channels controls the membrane potential. Thus, in some situations, a rise in the membrane potential can cause ion channels to open, thereby causing a further rise in the membrane potential.

An action potential occurs when this positive feedback cycle proceeds explosively. The time and amplitude trajectory of the action potential are determined by the biophysical properties of the voltage-gated ion channels that produce it. Several types of channels capable of producing the positive feedback necessary to generate an action potential do exist. Voltage-gated sodium channels are responsible for the fast action potentials involved in nerve conduction.

Slower action potentials in muscle cells and some types of neurons are generated by voltage-gated calcium channels. Each of these types comes in multiple variants, with different voltage sensitivity and different temporal dynamics. The most intensively studied type of voltage-dependent ion channels comprises the sodium channels involved in fast nerve conduction.

These are sometimes known as Hodgkin-Huxley sodium channels because they were first characterized by Alan Hodgkin and Andrew Huxley in their Nobel Prize-winning studies of the biophysics of the action potential, but can more conveniently be referred to as Na V channels.

The "V" stands for "voltage". An Na V channel has three possible states, known as deactivated , activated , and inactivated. The channel is permeable only to sodium ions when it is in the activated state. When the membrane potential is low, the channel spends most of its time in the deactivated closed state.

If the membrane potential is raised above a certain level, the channel shows increased probability of transitioning to the activated open state. The higher the membrane potential the greater the probability of activation. Once a channel has activated, it will eventually transition to the inactivated closed state. It tends then to stay inactivated for some time, but, if the membrane potential becomes low again, the channel will eventually transition back to the deactivated state.

This is only the population average behavior, however — an individual channel can in principle make any transition at any time. However, the likelihood of a channel's transitioning from the inactivated state directly to the activated state is very low: A channel in the inactivated state is refractory until it has transitioned back to the deactivated state.

The outcome of all this is that the kinetics of the Na V channels are governed by a transition matrix whose rates are voltage-dependent in a complicated way. Since these channels themselves play a major role in determining the voltage, the global dynamics of the system can be quite difficult to work out.

Hodgkin and Huxley approached the problem by developing a set of differential equations for the parameters that govern the ion channel states, known as the Hodgkin-Huxley equations.

These equations have been extensively modified by later research, but form the starting point for most theoretical studies of action potential biophysics. As the membrane potential is increased, sodium ion channels open, allowing the entry of sodium ions into the cell. This is followed by the opening of potassium ion channels that permit the exit 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 potential of the cell is higher than the cell's resting potential. The sodium channels close at the peak of the action potential, while potassium continues to leave the cell. The efflux of potassium ions decreases the membrane potential or hyperpolarizes the cell.

This results in a runaway condition whereby the positive feedback from the sodium current activates even more sodium channels. Thus, the cell fires , producing an action potential. Currents produced by the opening of voltage-gated channels in the course of an action potential are typically significantly larger than the initial stimulating current. Thus, the amplitude, duration, and shape of the action potential are determined largely by the properties of the excitable membrane and not the amplitude or duration of the stimulus.

This all-or-nothing property of the action potential sets it apart from graded potentials such as receptor potentials , electrotonic potentials , and synaptic potentials , which scale with the magnitude of the stimulus. A variety of action potential types exist in many cell types and cell compartments as determined by the types of voltage-gated channels, leak channels , channel distributions, ionic concentrations, membrane capacitance, temperature, and other factors.

The principal ions involved in an action potential are sodium and potassium cations; sodium ions enter the cell, and potassium ions leave, restoring equilibrium. Relatively few ions need to cross the membrane for the membrane voltage to change drastically.

The ions exchanged during an action potential, therefore, make a negligible change in the interior and exterior ionic concentrations.

The few ions that do cross are pumped out again by the continuous action of the sodium—potassium pump , which, with other ion transporters , maintains the normal ratio of ion concentrations across the membrane. Calcium cations and chloride anions are involved in a few types of action potentials, such as the cardiac action potential and the action potential in the single-cell alga Acetabularia , respectively.

Although action potentials are generated locally on patches of excitable membrane, the resulting currents can trigger action potentials on neighboring stretches of membrane, precipitating a domino-like propagation. In contrast to passive spread of electric potentials electrotonic potential , action potentials are generated anew along excitable stretches of membrane and propagate without decay. Regularly spaced unmyelinated patches, called the nodes of Ranvier , generate action potentials to boost the signal.

Known as saltatory conduction , this type of signal propagation provides a favorable tradeoff of signal velocity and axon diameter. Depolarization of axon terminals , in general, triggers the release of neurotransmitter into the synaptic cleft.

In addition, backpropagating action potentials have been recorded in the dendrites of pyramidal neurons , which are ubiquitous in the neocortex. A neuron 's ability to generate and propagate an action potential changes during development.

How much the membrane potential of a neuron changes as the result of a current impulse is a function of the membrane input resistance. As a cell grows, more channels are added to the membrane, causing a decrease in input resistance. A mature neuron also undergoes shorter changes in membrane potential in response to synaptic currents. Neurons from a ferret lateral geniculate nucleus have a longer time constant and larger voltage deflection at P0 than they do at P Immature neurons are more prone to synaptic depression than potentiation after high frequency stimulation.

In the early development of many organisms, the action potential is actually initially carried by calcium current rather than sodium current. The opening and closing kinetics of calcium channels during development are slower than those of the voltage-gated sodium channels that will carry the action potential in the mature neurons. The longer opening times for the calcium channels can lead to action potentials that are considerably slower than those of mature neurons.

During development, this time decreases to 1 ms. There are two reasons for this drastic decrease. First, the inward current becomes primarily carried by sodium channels. In order for the transition from a calcium-dependent action potential to a sodium-dependent action potential to proceed new channels must be added to the membrane. If Xenopus neurons are grown in an environment with RNA synthesis or protein synthesis inhibitors that transition is prevented.

If action potentials in Xenopus myocytes are blocked, the typical increase in sodium and potassium current density is prevented or delayed.

This maturation of electrical properties is seen across species. Xenopus sodium and potassium currents increase drastically after a neuron goes through its final phase of mitosis. Several types of cells support an action potential, such as plant cells, muscle cells, and the specialized cells of the heart in which occurs the cardiac action potential. However, the main excitable cell is the neuron , which also has the simplest mechanism for the action potential.

Neurons are electrically excitable cells composed, in general, of one or more dendrites, a single soma , a single axon and one or more axon terminals.

Dendrites are cellular projections whose primary function is to receive synaptic signals. Their protrusions, known as dendritic spines , are designed to capture the neurotransmitters released by the presynaptic neuron. They have a high concentration of ligand-gated ion channels. These spines have a thin neck connecting a bulbous protrusion to the dendrite.

This ensures that changes occurring inside the spine are less likely to affect the neighboring spines. The dendritic spine can, with rare exception see LTP , act as an independent unit.

The dendrites extend from the soma, which houses the nucleus , and many of the "normal" eukaryotic organelles. Unlike the spines, the surface of the soma is populated by voltage activated ion channels. These channels help transmit the signals generated by the dendrites. Emerging out from the soma is the axon hillock. This region is characterized by having a very high concentration of voltage-activated sodium channels.

In general, it is considered to be the spike initiation zone for action potentials, [14] i. Multiple signals generated at the spines, and transmitted by the soma all converge here. Immediately after the axon hillock is the axon. This is a thin tubular protrusion traveling away from the soma. The axon is insulated by a myelin sheath. Myelin is composed of either Schwann cells in the peripheral nervous system or oligodendrocytes in the central nervous system , both of which are types of glial cells.

Although glial cells are not involved with the transmission of electrical signals, they communicate and provide important biochemical support to neurons. This insulation prevents significant signal decay as well as ensuring faster signal speed. This insulation, however, has the restriction that no channels can be present on the surface of the axon. There are, therefore, regularly spaced patches of membrane, which have no insulation.

These nodes of Ranvier can be considered to be "mini axon hillocks", as their purpose is to boost the signal in order to prevent significant signal decay.

At the furthest end, the axon loses its insulation and begins to branch into several axon terminals. These presynaptic terminals, or synaptic boutons, are a specialized area within the axon of the presynaptic cell that contains neurotransmitters enclosed in small membrane-bound spheres called synaptic vesicles. Before considering the propagation of action potentials along axons and their termination at the synaptic knobs, it is helpful to consider the methods by which action potentials can be initiated at the axon hillock.

The basic requirement is that the membrane voltage at the hillock be raised above the threshold for firing. Action potentials are most commonly initiated by excitatory postsynaptic potentials from a presynaptic neuron. These neurotransmitters then bind to receptors on the postsynaptic cell. This binding opens various types of ion channels.

This opening has the further effect of changing the local permeability of the cell membrane and, thus, the membrane potential. If the binding increases the voltage depolarizes the membrane , the synapse is excitatory. If, however, the binding decreases the voltage hyperpolarizes the membrane , it is inhibitory.

Whether the voltage is increased or decreased, the change propagates passively to nearby regions of the membrane as described by the cable equation and its refinements. Typically, the voltage stimulus decays exponentially with the distance from the synapse and with time from the binding of the neurotransmitter. Some fraction of an excitatory voltage may reach the axon hillock and may in rare cases depolarize the membrane enough to provoke a new action potential. More typically, the excitatory potentials from several synapses must work together at nearly the same time to provoke a new action potential.

Their joint efforts can be thwarted, however, by the counteracting inhibitory postsynaptic potentials. Neurotransmission can also occur through electrical synapses. The free flow of ions between cells enables rapid non-chemical-mediated transmission. Rectifying channels ensure that action potentials move only in one direction through an electrical synapse. The amplitude of an action potential is independent of the amount of current that produced it. In other words, larger currents do not create larger action potentials.

Therefore, action potentials are said to be all-or-none signals, since either they occur fully or they do not occur at all. In sensory neurons , an external signal such as pressure, temperature, light, or sound is coupled with the opening and closing of ion channels , which in turn alter the ionic permeabilities of the membrane and its voltage. This short article about biology can be made longer. You can help Wikipedia by adding to it. Retrieved from " https: Views Read Change Change source View history.

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After attacking and capturing the Dalmatian cities under Byzantine control, the Venetians landed in the island of Euboea but were expelled by imperial troops, and then occupied the island of Chios to spend the winter. The Venetians sent envoys to negotiate, but Manuel allowed them to drag on until his own counterstroke, ships under Kontostephanos' command, was ready. In the meantime, the Venetians suffered of disease on Chios. Kontostephanos pursued them, but while the Venetians sailed north, raiding the islands of Thasos , Lesbos and Skyros , he assumed they would sail back westwards, and directed his fleet to Cape Malea.

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