what causes voltage gated sodium channels to close

Introduction

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Opening of Voltage Gated Channels Produces Action Potentials

The subunits of voltage-gated ion channels change conformation in accordance with membrane potential. This can result in the opening of a pore that allows a specific ion to pass through the membrane.

Two types of voltage-gated channels play a role in producing action potentials: those that let sodium to cross the membrane (voltage-gated sodium channels ) and those that allow potassium to cantankerous the membrane ( voltage-gated potassium channels ).

Voltage-gated channels are not normally nowadays in the dendrites or the soma, but are concentrated in the initial segment of the axon ( axon hillock ). Both inhibitory and excitatory postsynaptic potentials are summed in the axon hillock. If the inside of the axon hillock is sufficiently depolarized (becomes less negatively charged), the Na+ channels open and allow Na+ to enter the neuron. Since Na+ concentration is low inside the jail cell (due to the actions of the sodium-potassium pump ) and the inside of the cell is negatively charged, Na+ rushes from the outside to the inside of the cell.

Voltage-gated Na+ channels have two gates: an activation gate and an inactivation gate. The activation gate opens quickly when the membrane is depolarized, and allows Na+ to enter. Nevertheless, the same change in membrane potential too causes the inactivation gate to close. The closure of the inactivation gate is slower than the opening of the activation gate. As a upshot, the channel is open for a very cursory time (from the opening of the activation gate to the closure of the inactivation gate). Another important characteristic of the sodium channel inactivation process is that the inactivation gate volition not reopen until the membrane potential returns to the original resting membrane potential level. Therefore, information technology is not possible for the sodium channels to open again without start repolarizing the nerve fiber.

When the Na+ channels are open at the axon hillock, the local membrane potential speedily becomes positive. It approaches the equilibrium potential for Na+, but does not attain it before the channels inactivate. When the membrane at the axon hillock becomes depolarized, an opening of voltage-gated K+ channels also occurs. Since K+ is in loftier concentration inside the neuron, Grand+ diffuses outward through the channel. Even so, because of a filibuster in opening the Yard+ channels, they open at near the same time that the Na+ channels are closing because of inactivation. Thus, the decrease in sodium entry to the cell and the simultaneous increment in potassium exit from the prison cell combine to speed the repolarization process, leading to recovery of the resting membrane potential.

This figure summarizes the events that occur during and after the activeness potential. The bottom of the figure shows the changes in membrane conductance for Na+ and Chiliad+ ions. During the resting state, the conductance for Thou+ ions is 50–100 times greater than the conductance for Na+ ions. This is due to leakage of Grand+ ions through the leak channels. At the onset of the activeness potential, Na+ sodium channels open up and permit up to a 5000-fold increment in Na+ conductance. The inactivation process then closes the Na+ channels. The onset of the action potential besides triggers voltage gating of the K+ channels, causing them to open at the time the Na+ channels close. This produces a 30-fold increase in Grand+ conductance. At the end of the action potential, the return of the membrane potential to the negative state causes the 1000+ channels to shut slowly. A common feature of activeness potentials is an afterhyperpolarization . As noted in the membrane potential module , the main factor that sets the resting membrane potential is the move of K+ ions through leak channels. When the voltage-gated K+ channels are open up, the conductance for K+ is higher than during the resting country. As a event, the membrane potential approaches the equilibrium potential for K+ (is more negative than in the resting state), resulting in the afterhyperpolarization. As soon every bit the voltage-gated K+ channels close, the conductance for Thousand+ is reduced and the membrane potential returns to normal resting values.

Note that after the resting membrane potential is restored, a short period elapses before the inactivation gates of the voltage-gated Na+ channels open. While the inactivation gate is closed, it is impossible for a new activeness potential to be elicited. This flow is called the absolute refractory period.

As noted above, the voltage-gated One thousand+ channels close slowly after the membrane has been repolarized. Consequently, the 1000+ conductance is higher (and the neuronal membrane is more hyperpolarized) at the end of the activity than in the normal resting country. As a result, it is more difficult to generate the amount of depolarization needed to open the activation gates. This period of higher K+ conductance at the terminate of an action potential results in a relative refractory period, during which it is possible to elicit an action potential, although a strong excitation is need to exercise so.

Saltatory Conduction in Myelinated Axons

Many neurons have myelin surrounding the axon. Myelin is a fatty white substance deposited by glial cells that insulates the axon, decreasing the leak of current through the axonal membrane. The voltage-gated channels described above are located between side by side myelin sheaths. An unmyelinated area of membrane at the gaps between myelin sheaths, which contains voltage-gated channels, is chosen a node of Ranvier .

Myelination allows a bolus of sodium that enters through voltage-gated Na+ channels to move quickly downwardly the axon without leaking out very much. Another action potential occurs at the next node of Ranvier downward the axon, refreshing the process. As such, the action potential appears to "leap" betwixt the nodes of Ranvier, in a process called saltatory conduction .

Saltatory conduction allows electrical nervus signals to exist propagated long distances at high rates without whatsoever degradation of the betoken. In add-on, the process is energy-efficient, as perturbations in the normal compartmentalization of Na+ and K+ only occur at the nodes of Ranvier. Bear in heed that after an action potential, the sodium-potassium pump has to restore the normal ionic balance across the membrane. Minimizing the demand to do this reduces ATP expenditure.

Now you should be able to understand that the refractory period for axons described in the section higher up has a very applied physiological purpose: information technology assures that action potentials move in one direction down the axon. When an action potential is generated at one node of Ranvier, the previous node is still in a refractory period. Although sodium ions entering at a node diffuse in both directions down the axon, the previously-activated node cannot generate an activeness potential. This is primal in assuring that an excitatory input to a neuron does not event in a reverberating series of action potentials.

Unmyelinated Axons Acquit Action Potentials Slowly

In contrast to myelinated axons, unmyelinated neurons must "refresh" the activeness potential in every successive patch of membrane. Thus, a repeated entry of Na+ ions and efflux of One thousand+ ions occurs down the axon. The ionic redistribution is restored to the resting country by the sodium-potassium pump, just this requires a big amount of energy.

This may be the reason why unmyelinated axons accept a small bore. If an unmyelinated axon was of big diameter, the expanse would exist large and many voltage-gated channels would be needed on the surface. When an activeness potential occurred, the move of ions would be large, and a tremendous amount of ATP would be needed to fuel the activeness of the sodium-potassium pump to restore ionic balance.

Two major factors govern how quickly an activity potential moves downs an axon:

• its diameter
• how heavily myelinated it is

In general, the largest axons are also the about heavily myelinated, and propagate action potentials very speedily. The smallest axons are unmyelinated and propagate activity potentials slowly.

How practice the amount of myelination and the diameter of an axon determine its conduction velocity?

Allow's turn to the KhanAcademy for an explanation.

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Although the action potentials of most neurons resemble those described to a higher place, some neurons have activity potentials with different properties.

Every bit an example, cerebellar Purkinje cells produce complex spikes, which are very broad and complicated activeness potentials.

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Source: http://pittmedneuro.com/actionpotentials.html

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