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Is the Resting Potential and Action Potential Thresholds the same across all neurons in a network?

Is the Resting Potential and Action Potential Thresholds the same across all neurons in a network?


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Does the action potential and resting potential of a given neuron differ from another neuron within the same network or is it constant? If not what determines and affects these potentials and can they change overtime? If so what factor contribute to this change and how?


In short no. The speed at which and Action Potential (AP) occurs, resting membrane potential, and threshold to AP all vary across types of neutron. See the graph below (Bean, 2007)

The reasons for these differences are various, as you will see if you read the referenced article, which I highly recommend as everything I write from here is based upon it. The main factors influencing AP differences are firstly that the classical AP diagram is based on an isolate squid giant axon (not neuron) in a superficial environment.

When we investigate neurons in mammals we investigate them relative to surrounding neurons, which influences chemoelectric potentials and subsequently APs. Furthermore neurons aren't uniform in shape which also has an influence. Secondly voltage gating varies within and between ions gates in the neural membranes for instance "the kinetics of sodium currents differ in detail between different types of neurons62 and, remarkably, even between different regions of the same neuron, with sodium channels in hippocampal mossy fibre boutons (formed by the axons of granule cells of the dentate gyrus) inactivating twice as fast as the sodium channels in the granule cell sonata" Bean (2007). Potassium channels appear to lack uniformity as well. See below for difference in voltages across ion channels between neurons.

And there are other factors as well of course, such as frequency of activation influencing voltage required to depolarise. Depolarisation rates, and differences between fast spiking neurons, such as purkinji, and others.

Overall the brain is not uniform, despite what you may learn or have learnt in text books in classes. This is done to ease learning, can you imagine trying to learnt this without the basics? However this fundamental research has important implications for neural imaging, psychopharmatuics, and of course cognitive processes such as speed of processing etc.

In case you can't access the reference… The referenced journal article is a brilliant review in nature about this exact topic, its called "The action potential in mammalian central neurons" By Bruce P Bean


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Contents

Function

Nearly all cells from animals, plants and fungi function as batteries, in the sense that they maintain a voltage difference between the interior and the exterior of the cell, with the interior being the negative pole of the battery. The voltage of a cell is usually measured in millivolts (mV), or thousandths of a volt. A typical voltage for an animal cell is –70 mV—approximately one-fifteenth of a volt. Because cells are so small, voltages of this magnitude give rise to very strong electric forces within the cell membrane.

In the majority of cells, the voltage changes very little over time. There are some types of cells, however, that are electrically active in the sense that their voltages fluctuate. In some of these, the voltages sometimes show very rapid up-and-down fluctuations that have a stereotyped form: These up-and-down cycles are known as action potentials. The durations of action potentials vary across a wide range. In brain cells of animals, the entire up-and-down cycle may take place in less than a thousandth of a second. In other types of cells, the cycle may last for several seconds.

The electrical properties of an animal cell are determined by the structure of the membrane that surrounds it. A cell membrane consists of a layer of lipid molecules with larger protein molecules embedded in it. The lipid layer is highly resistant to movement of electrically charged ions, so it functions mainly as an insulator. The large membrane-embedded molecules, in contrast, provide channels through which ions can pass across the membrane, and some of the large molecules are capable of actively moving specific types of ions from one side of the membrane to the other.

Process in a typical neuron

All cells in animal body tissues are electrically polarized — in other words, they maintain a voltage difference across the cell's plasma membrane, known as the membrane potential. This electrical polarization results from a complex interplay between protein structures embedded in the membrane called ion pumps and ion channels. In neurons, the types of ion channels in the membrane usually vary across different parts of the cell, giving the dendrites, axon, and cell body different electrical properties. As a result, some parts of the membrane of a neuron may be excitable (capable of generating action potentials), whereas others are not. The most excitable part of a neuron is usually the axon hillock (the point where the axon leaves the cell body), but the axon and cell body are also excitable in most cases.

Each excitable patch of membrane has two important levels of membrane potential: the resting potential, which is the value the membrane potential maintains as long as nothing perturbs the cell, and a higher value called the threshold 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, often reaching as high as +100 mV, 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 that is, 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 less than a thousandth of a second. Many types of neurons emit action potentials constantly at rates of up to 10-100 per second some types, however, are much quieter, and may go for minutes or longer without emitting any action potentials.


What is the Difference Between Resting Potential and Action Potential

The main difference between resting potential and action potential is that resting potential is the resting voltage or the membrane potential of a non-excited nerve cell at rest, whereas action potential is the membrane potential of an excited nerve cell during the transmission of a nerve impulse . Furthermore, resting potential is -70 mV while action potential is +40 mV.

Resting potential and action potential are two types of membrane potentials that occur on the axon membrane of nerve cells. Resting potential is relatively static while action potential is a rapid rise and fall when considering a particular location on the membrane.

Key Areas Covered

Key Terms

Action Potential, Depolarization, Hyperpolarization, Potassium Channels, Resting Potential, Sodium Channels


Resting potential

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Resting potential, the imbalance of electrical charge that exists between the interior of electrically excitable neurons (nerve cells) and their surroundings. The resting potential of electrically excitable cells lies in the range of −60 to −95 millivolts (1 millivolt = 0.001 volt), with the inside of the cell negatively charged. If the inside of a cell becomes more electronegative (i.e., if the potential is made greater than the resting potential), the membrane or the cell is said to be hyperpolarized. If the inside of the cell becomes less negative (i.e., the potential decreases below the resting potential), the process is called depolarization.

During the transmission of nerve impulses, the brief depolarization that occurs when the inside of the nerve cell fibre becomes positively charged is called the action potential. This brief alteration of polarization, thought to be caused by the shifting of positively charged sodium ions from the outside to the inside of the cell, results in the transmission of nerve impulses. After depolarization, the cell membrane becomes relatively permeable to positively charged potassium ions, which diffuse outward from the inside of the cell, where they normally occur in rather high concentration. The cell then resumes the negatively charged condition characteristic of the resting potential.

This article was most recently revised and updated by Kara Rogers, Senior Editor.


Action Potential Propagation

Action potential propagation describes how an impulse moves along a cell membrane, most commonly the axon of a nerve cell. We already know that many neurons are incredibly long. In order to ensure an action potential continues without being lost or without the amount of depolarization being reduced to below threshold (some ions will continue to move out of the cell via leakage channels), the action potential needs to continue along the axon. To make this as efficient as possible in neurons that do not have an insulating myelin sheath, sections of the cell membrane depolarize at a time, pulling the action potential in one direction towards a target cell. This section-by-section movement is action potential propagation. First initiation, then propagation.

Think of a single ion channel inside a membrane that has received a message from cAMP to open and let sodium ions into the cell. If the nerve cell in question is located in the neck of the giraffe, how does it keep enough sodium flowing in and stay above the threshold levels as it moves along? While more than one ion channel will be affected by cAMP, how will the action potential move in one direction all the way to the nerve cell synapse? This is where negative and positive attraction comes in.

As sodium ions flow in, the area of the cell membrane close to the ion channel will start to become more positive. It takes time for atoms to diffuse completely into the cytoplasm and a nerve needs lightening speed. In the short space of time it has been given, the threshold charge only exists slightly to the left and right of the ion channel. Imagine a single plus under an ion channel surrounded by minus signs.

Due to positive and negative attraction, that plus is pulled in the direction of the next ion channel it is a positive charge, so it slightly neutralizes the negative charge that attracts it. The region immediately under the first ion channel has now lost its positive charge by passing it along and becomes negative once more. Every time the positive charge arrives at the next point, the neighboring negative charge pulls it closer.

This change in voltage opens other sodium channels that do not rely on cAMP but on the change in charge – voltage-gated sodium channels. This way, any leakage of sodium ions is compensated for. An action potential is, therefore, like a string of light bulbs that are lit one at a time in a single direction, one after the other. The lighted bulb indicates the positive charge.

After depolarization comes repolarization. As we know that depolarization means an increasing (positive) difference in charge at the inside of the cell membrane, we can then surmise that repolarization is the opposite – the return of the inner membrane to its resting potential by returning to the original negative charge. If depolarization is an uphill line, the repolarization line points down. This can only happen with potassium ions. Voltage-dependent potassium ion channels open in the presence of a positive electrical charge inside the cell and help K + ions to move out. At the same time, the sodium ion channels close. With all of these positive ions either leaving the cell or unable to enter, the resting potential is achieved.

In fact, the resting potential is completely passed by. At first, the electrical charge of the inner cell membrane becomes lower than the resting potential. When the charge is lower than -70 mV, we speak of hyperpolarization. This is because the sodium and potassium channels are unable to immediately close once -70 mV has been achieved.

In peripheral neurons, action potential propagation occurs at the nodes of Ranvier between individual Schwann cells. Schwann cells cover the axon of the neuron in myelin, a form of insulation that stops voltage-dependent sodium channels from letting sodium ions in. Even though this insulation layer also reduces leakage, the amount of depolarization would reduce as sodium ions diffused away from the immediate area. A nerve impulse would initiate but fade away.

In order to prevent this, unmyelinated nodes between the Schwann cells mean ion channels can let sodium ions in. In this case, each node of Ranvier is a light bulb with a positive charge, sending the message along an axon. The inner positive to negative pull also ensures the action potential continues to travel forward.

But how does an action potential travels in one direction? How is it that the pull of the next negative charge brings the action potential forward and not backward?

One-way action potentials are the result of the ion channel refractory period. Once an ion channel has opened, it cannot open again for a period of time – approximately one to two milliseconds. This is enough to ensure that the next voltage-dependent ion channel in the chain reacts to the change in charge and allows the next batch of Na + ions to flow inside the cell, raising the charge at the inner membrane around that channel.


Contents

Figure 1: Intra- and extracellular ion concentrations (mmol/L)
Element Ion Extracellular Intracellular Ratio
Sodium Na + 135 - 145 10 14:1
Potassium K + 3.5 - 5.0 155 1:30
Chloride Cl − 95 - 110 10 - 20 4:1
Calcium Ca 2+ 2 10 −4 2 x 10 4 :1
Although intracellular Ca 2+ content is about 2 mM, most of this is bound or sequestered in intracellular organelles (mitochondria and sarcoplasmic reticulum). [5]

Similar to skeletal muscle, the resting membrane potential (voltage when the cell is not electrically excited) of ventricular cells, is around -90 millivolts (mV 1 mV = 0.001 V) i.e. the inside of the membrane is more negative than the outside. The main ions found outside the cell at rest are sodium (Na + ), and chloride (Cl − ), whereas inside the cell it is mainly potassium (K + ). [6]

The action potential begins with the voltage becoming more positive this is known as depolarization and is mainly due to the opening of sodium channels that allow Na + to flow into the cell. After a delay (known as the absolute refractory period see below), termination of the action potential then occurs, as potassium channels open, allowing K + to leave the cell and causing the membrane potential to return to negative, this is known as repolarization. Another important ion is calcium (Ca 2+ ), which can be found outside of the cell as well as inside the cell, in a calcium store known as the sarcoplasmic reticulum (SR). Release of Ca 2+ from the SR, via a process called calcium-induced calcium release, is vital for the plateau phase of the action potential (see phase 2, below) and is a fundamental step in cardiac excitation-contraction coupling. [7]

There are important physiological differences between the cells that spontaneously generate the action potential (pacemaker cells e.g. SAN) and those that simply conduct it (non-pacemaker cells e.g. ventricular myocytes). The specific differences in the types of ion channels expressed and mechanisms by which they are activated results in differences in the configuration of the action potential waveform, as shown in figure 2.

The standard model used to understand the cardiac action potential is that of the ventricular myocyte. Outlined below are the five phases of the ventricular myocyte action potential, with reference also to the SAN action potential.

Phase 4 Edit

In the ventricular myocyte, phase 4 occurs when the cell is at rest, in a period known as diastole. In the standard non-pacemaker cell the voltage during this phase is more or less constant, at roughly -90 mV. [8] The resting membrane potential results from the flux of ions having flowed into the cell (e.g. sodium and calcium) and the ions having flowed out of the cell (e.g. potassium, chloride and bicarbonate) being perfectly balanced.

The leakage of these ions across the membrane is maintained by the activity of pumps which serve to keep the intracellular concentration more or less constant, so for example, the sodium (Na + ) and potassium (K + ) ions are maintained by the sodium-potassium pump which uses energy (in the form of adenosine triphosphate (ATP)) to move three Na + out of the cell and two K + into the cell. Another example is the sodium-calcium exchanger which removes one Ca 2+ from the cell for three Na + into the cell. [9]

During this phase the membrane is most permeable to K + , which can travel into or out of cell through leak channels, including the inwardly rectifying potassium channel. [10] Therefore, the resting membrane potential is mainly determined by K + equilibrium potential and can be calculated using the Goldman-Hodgkin-Katz voltage equation.

However, pacemaker cells are never at rest. In these cells, phase 4 is also known as the pacemaker potential. During this phase, the membrane potential slowly becomes more positive, until it reaches a set value (around -40 mV known as the threshold potential) or until it is depolarized by another action potential, coming from a neighboring cell.

The pacemaker potential is thought to be due to a group of channels, referred to as HCN channels (Hyperpolarization-activated cyclic nucleotide-gated). These channels open at very negative voltages (i.e. immediately after phase 3 of the previous action potential see below) and allow the passage of both K + and Na + into the cell. Due to their unusual property of being activated by very negative membrane potentials, the movement of ions through the HCN channels is referred to as the funny current (see below). [11]

Another hypothesis regarding the pacemaker potential is the ‘calcium clock’. Here, calcium is released from the sarcoplasmic reticulum, within the cell. This calcium then increases activation of the sodium-calcium exchanger resulting in the increase in membrane potential (as a +3 charge is being brought into the cell (by the 3Na + ) but only a +2 charge is leaving the cell (by the Ca 2+ ) therefore there is a net charge of +1 entering the cell). This calcium is then pumped back into the cell and back into the SR via calcium pumps (including the SERCA). [12]

Phase 0 Edit

This phase consists of a rapid, positive change in voltage across the cell membrane (depolarization) lasting less than 2 ms, in ventricular cells and 10/20 ms in SAN cells. [13] This occurs due to a net flow of positive charge into the cell.

In non-pacemaker cells (i.e. ventricular cells), this is produced predominantly by the activation of Na + channels, which increases the membrane conductance (flow) of Na + (gNa). These channels are activated when an action potential arrives from a neighbouring cell, through gap junctions. When this happens, the voltage within the cell increases slightly. If this increased voltage reaches a certain value (threshold potential

-70 mV) it causes the Na + channels to open. This produces a larger influx of sodium into the cell, rapidly increasing the voltage further (to

+50 mV [6] i.e. towards the Na + equilibrium potential). However, if the initial stimulus is not strong enough, and the threshold potential is not reached, the rapid sodium channels will not be activated and an action potential will not be produced this is known as the all-or-none law. [14] [15] The influx of calcium ions (Ca 2+ ) through L-type calcium channels also constitutes a minor part of the depolarisation effect. [16] The slope of phase 0 on the action potential waveform (see figure 2) represents the maximum rate of voltage change, of the cardiac action potential and is known as dV/dtmax.

In pacemaker cells (e.g. sinoatrial node cells), however, the increase in membrane voltage is mainly due to activation of L-type calcium channels. These channels are also activated by an increase in voltage, however this time it is either due to the pacemaker potential (phase 4) or an oncoming action potential. The L-type calcium channels activate towards the end of the pacemaker potential (and therefore contribute to the latter stages of the pacemaker potential). The L-type calcium channels are activated more slowly than the sodium channels, in the ventricular cell, therefore, the depolarization slope in the pacemaker action potential waveform is less steep than that in the non-pacemaker action potential waveform. [8] [17]

Phase 1 Edit

This phase begins with the rapid inactivation of the Na + channels by the inner gate (inactivation gate), reducing the movement of sodium into the cell. At the same time potassium channels (called Ito1) open and close rapidly, allowing for a brief flow of potassium ions out of the cell, making the membrane potential slightly more negative. This is referred to as a ‘notch’ on the action potential waveform. [8]

There is no obvious phase 1 present in pacemaker cells.

Phase 2 Edit

This phase is also known as the "plateau" phase due to the membrane potential remaining almost constant, as the membrane slowly begins to repolarize. This is due to the near balance of charge moving into and out of the cell. During this phase delayed rectifier potassium channels allow potassium to leave the cell while L-type calcium channels (activated by the flow of sodium during phase 0), allow the movement of calcium ions into the cell. These calcium ions bind to and open more calcium channels (called ryanodine receptors) located on the sarcoplasmic reticulum within the cell, allowing the flow of calcium out of the SR. These calcium ions are responsible for the contraction of the heart. Calcium also activates chloride channels called Ito2, which allow Cl − to enter the cell. The movement of Ca 2+ opposes the repolarizing voltage change caused by K + and Cl − [ citation needed ] . As well as this the increased calcium concentration increases the activity of the sodium-calcium exchanger, and the increase in sodium entering the cell increases activity of the sodium-potassium pump. The movement of all of these ions results in the membrane potential remaining relatively constant. [18] [8] This phase is responsible for the large duration of the action potential and is important in preventing irregular heartbeat (cardiac arrhythmia).

There is no plateau phase present in pacemaker action potentials.

Phase 3 Edit

During phase 3 (the "rapid repolarization" phase) of the action potential, the L-type Ca 2+ channels close, while the slow delayed rectifier (IKs) K + channels remain open as more potassium leak channels open. This ensures a net outward positive current, corresponding to negative change in membrane potential, thus allowing more types of K + channels to open. These are primarily the rapid delayed rectifier K + channels (IKr) and the inwardly rectifying K + current, IK1. This net outward, positive current (equal to loss of positive charge from the cell) causes the cell to repolarize. The delayed rectifier K + channels close when the membrane potential is restored to about -85 to -90 mV, while IK1 remains conducting throughout phase 4, which helps to set the resting membrane potential [19]

Ionic pumps as discussed above, like the sodium-calcium exchanger and the sodium-potassium pump restore ion concentrations back to balanced states pre-action potential. This means that the intracellular calcium is pumped out, which was responsible for cardiac myocyte contraction. Once this is lost the contraction stops and myocytic cells relax, which in turn relaxes the heart muscle.

During this phase, the action potential fatefully commits to repolarisation. This begins with the closing of the L-type Ca 2+ channels, while the K + channels (from phase 2) remain open. The main potassium channels involved in repolarization are the delayed rectifiers (IKr) and (IKs) as well as the inward rectifier (IK1). Overall there is a net outward positive current, that produces negative change in membrane potential. [18] The delayed rectifier channels close when the membrane potential is restored to resting potential, whereas the inward rectifier channels and the ion pumps remain active throughout phase 4, resetting the resting ion concentrations. This means that the calcium used for muscle contraction, is pumped out of the cell, resulting in muscle relaxation.

In the sinoatrial node, this phase is also due to the closure of the L-type calcium channels, preventing inward flux of Ca 2+ and the opening of the rapid delayed rectifier potassium channels (IKr). [20]

Cardiac cells have two refractory periods, the first from the beginning of phase 0 until part way through phase 3 this is known as the absolute refractory period during which it is impossible for the cell to produce another action potential. This is immediately followed, until the end of phase 3, by a relative refractory period, during which a stronger-than-usual stimulus is required to produce another action potential. [21] [22]

These two refractory periods are caused by changes in the states of sodium and potassium channels. The rapid depolarization of the cell, during phase 0, causes the membrane potential to approach sodium's equilibrium potential (i.e. the membrane potential at which sodium is no longer drawn into or out of the cell). As the membrane potential becomes more positive, the sodium channels then close and lock, this is known as the "inactivated" state. During this state the channels cannot be opened regardless of the strength of the excitatory stimulus—this gives rise to the absolute refractory period. The relative refractory period is due to the leaking of potassium ions, which makes the membrane potential more negative (i.e. it is hyperpolarised), this resets the sodium channels opening the inactivation gate, but still leaving the channel closed. This means that it is possible to initiate an action potential, but a stronger stimulus than normal is required. [23]

Gap junctions allow the action potential to be transferred from one cell to the next (they are said to electrically couple neighbouring cardiac cells). They are made from the connexin family of proteins, that form a pore through which ions (including Na + , Ca 2+ and K + ) can pass. As potassium is highest within the cell, it is mainly potassium that passes through. This increased potassium in the neighbour cell causes the membrane potential to increase slightly, activating the sodium channels and initiating an action potential in this cell. (A brief chemical gradient driven efflux of Na+ through the connexon at peak depolarization causes the conduction of cell to cell depolarization, not potassium.) [24] These connections allow for the rapid conduction of the action potential throughout the heart and are responsible for allowing all of the cells in the atria to contract together as well as all of the cells in the ventricles. [25] Uncoordinated contraction of heart muscles is the basis for arrhythmia and heart failure. [26]

Figure 3: Major currents during the cardiac ventricular action potential [27]
Current (I) α subunit protein α subunit gene Phase / role
Na + INa NaV1.5 SCN5A [28] 0
Ca 2+ ICa(L) CaV1.2 CACNA1C [29] 0-2
K + Ito1 KV4.2/4.3 KCND2/KCND3 1, notch
K + IKs KV7.1 KCNQ1 2,3
K + IKr KV11.1 (hERG) KCNH2 3
K + IK1 Kir2.1/2.2/2.3 KCNJ2/KCNJ12/KCNJ4 3,4
Na + , Ca 2+ INaCa 3Na + -1Ca 2+ -exchanger NCX1 (SLC8A1) ion homeostasis
Na + , K + INaK 3Na + -2K + -ATPase ATP1A ion homeostasis
Ca 2+ IpCa Ca 2+ -transporting ATPase ATP1B ion homeostasis

Ion channels are proteins, that change shape in response to different stimuli to either allow or prevent the movement of specific ions across a membrane (they are said to be selectively permeable). Stimuli, which can either come from outside the cell or from within the cell, can include the binding of a specific molecule to a receptor on the channel (also known as ligand-gated ion channels) or a change in membrane potential around the channel, detected by a sensor (also known as voltage-gated ion channels) and can act to open or close the channel. The pore formed by an ion channel is aqueous (water filled) and allows the ion to rapidly travel across the membrane. [30] Ion channels can be selective for specific ions, so there are Na + , K + , Ca 2+ , and Cl − specific channels. They can also be specific for a certain charge of ions (i.e. positive or negative). [31]

Each channel is coded by a set of DNA instructions that tell the cell how to make it. These instructions are known as a gene. Figure 3 shows the important ion channels involved in the cardiac action potential, the current (ions) that flows through the channels, their main protein subunits (building blocks of the channel), some of their controlling genes that code for their structure and the phases they are active during the cardiac action potential. Some of the most important ion channels involved in the cardiac action potential are described briefly below.

Hyperpolarisation activated cyclic nucleotide gated (HCN) channels Edit

Located mainly in pacemaker cells, these channels become active at very negative membrane potentials and allow for the passage of both Na + and K + into the cell (this movement is known as a funny current, If). These poorly selective, cation (positively charged ions) channels conduct more current as the membrane potential becomes more negative (hyperpolarised). The activity of these channels in the SAN cells causes the membrane potential to depolarise slowly and so they are thought to be responsible for the pacemaker potential. Sympathetic nerves directly affect these channels, resulting in an increased heart rate (see below). [32] [11]

The fast Na + channel Edit

These sodium channels are voltage-dependent, opening rapidly due to depolarization of the membrane, which usually occurs from neighboring cells, through gap junctions. They allow for a rapid flow of sodium into the cell, depolarizing the membrane completely and initiating an action potential. As the membrane potential increases, these channels then close and lock (become inactive). Due to the rapid influx sodium ions (steep phase 0 in action potential waveform) activation and inactivation of these channels happens almost at exactly the same time. During the inactivation state, Na + cannot pass through (absolute refractory period). However they begin to recover from inactivation as the membrane potential becomes more negative (relative refractory period).

Potassium channels Edit

The two main types of potassium channels in cardiac cells are inward rectifiers and voltage-gated potassium channels.

Inwardly rectifying potassium channels (Kir) favour the flow of K + into the cell. This influx of potassium, however, is larger when the membrane potential is more negative than the equilibrium potential for K + (

-90 mV). As the membrane potential becomes more positive (i.e. during cell stimulation from a neighbouring cell), the flow of potassium into the cell via the Kir decreases. Therefore, Kir is responsible for maintaining the resting membrane potential and initiating the depolarization phase. However, as the membrane potential continues to become more positive, the channel begins to allow the passage of K + out of the cell. This outward flow of potassium ions at the more positive membrane potentials means that the Kir can also aid the final stages of repolarisation. [33] [34]

The voltage-gated potassium channels (Kv) are activated by depolarization. The currents produced by these channels include the transient out potassium current Ito1. This current has two components. Both components activate rapidly, but Ito,fast inactivates more rapidly than Ito, slow. These currents contribute to the early repolarization phase (phase 1) of the action potential.

Another form of voltage-gated potassium channels are the delayed rectifier potassium channels. These channels carry potassium currents which are responsible for the plateau phase of the action potential, and are named based on the speed at which they activate: slowly activating IKs, rapidly activating IKr and ultra-rapidly activating IKur. [35]

Calcium channels Edit

There are two voltage-gated calcium channels within cardiac muscle: L-type calcium channels ('L' for Long-lasting) and T-type calcium channels ('T' for Transient, i.e. short). L-type channels are more common and are most densely populated within the t-tubule membrane of ventricular cells, whereas the T-type channels are found mainly within atrial and pacemaker cells, but still to a lesser degree than L-type channels.

These channels respond to voltage changes across the membrane differently: L-type channels are activated by more positive membrane potentials, take longer to open and remain open longer than T-type channels. This means that the T-type channels contribute more to depolarization (phase 0) whereas L-type channels contribute to the plateau (phase 2). [36]

Electrical activity that originates from the sinoatrial node is propagated via the His-Purkinje network, the fastest conduction pathway within the heart. The electrical signal travels from the sinoatrial node (SAN), which stimulates the atria to contract, to the atrioventricular node (AVN) which slows down conduction of the action potential, from the atria to the ventricles. This delay allows the ventricles to fully fill with blood before contraction. The signal then passes down through a bundle of fibres called the bundle of His, located between the ventricles, and then to the purkinje fibers at the bottom (apex) of the heart, causing ventricular contraction. This is known as the electrical conduction system of the heart, see figure 4.

Other than the SAN, the AVN and purkinje fibres also have pacemaker activity and can therefore spontaneously generate an action potential. However, these cells usually do not depolarize spontaneously, simply because, action potential production in the SAN is faster. This means that before the AVN or purkinje fibres reach the threshold potential for an action potential, they are depolarized by the oncoming impulse from the SAN [37] This is called "overdrive suppression". [38] Pacemaker activity of these cells is vital, as it means that if the SAN were to fail, then the heart could continue to beat, albeit at a lower rate (AVN= 40-60 beats per minute, purkinje fibres = 20-40 beats per minute). These pacemakers will keep a patient alive until the emergency team arrives.

An example of premature ventricular contraction, is the classic athletic heart syndrome. Sustained training of athletes causes a cardiac adaptation where the resting SAN rate is lower (sometimes around 40 beats per minute). This can lead to atrioventricular block, where the signal from the SAN is impaired in its path to the ventricles. This leads to uncoordinated contractions between the atria and ventricles, without the correct delay in between and in severe cases can result in sudden death. [39]

Regulation by the autonomic nervous system Edit

The speed of action potential production in pacemaker cells is affected, but not controlled by the autonomic nervous system.

The sympathetic nervous system (nerves dominant during the bodies fight or flight response) increase heart rate (positive chronotropy), by decreasing the time to produce an action potential in the SAN. Nerves from the spinal cord release a molecule called noradrenaline, which binds to and activates receptors on the pacemaker cell membrane called β1 adrenoceptors. This activates a protein, called a Gs-protein (s for stimulatory). Activation of this G-protein leads to increased levels of cAMP in the cell (via the cAMP pathway). cAMP binds to the HCN channels (see above), increasing the funny current and therefore increasing the rate of depolarization, during the pacemaker potential. The increased cAMP also increases the opening time of L -type calcium channels, increasing the Ca 2+ current through the channel, speeding up phase 0. [40]

The parasympathetic nervous system (nerves dominant while the body is resting and digesting) decreases heart rate (negative chronotropy), by increasing the time taken to produce an action potential in the SAN. A nerve called the vagus nerve, that begins in the brain and travels to the sinoatrial node, releases a molecule called acetylcholine (ACh) which binds to a receptor located on the outside of the pacemaker cell, called an M2 muscarinic receptor. This activates a Gi-protein (I for inhibitory), which is made up of 3 subunits (α, β and γ) which, when activated, separate from the receptor. The β and γ subunits activate a special set of potassium channels, increasing potassium flow out of the cell and decreasing membrane potential, meaning that the pacemaker cells take longer to reach their threshold value. [41] The Gi-protein also inhibits the cAMP pathway therefore reducing the sympathetic effects caused by the spinal nerves. [42]


Factors Affecting the Speed of Nerve Impulse

Following are some major factors that affect the speed of nerve impulse:

Myelin Sheath

Myelin sheath is present around the neuron and functions as an electrical insulator. Due to this sheath, an action potential is not formed on the surface of the neuron. This Myelin sheath has regular gaps, where it is not present, called nodes of Ranvier. An action potential can form at these gaps and impulse will jump from node to node by saltatory conduction. This can be a factor for increasing the speed of nerve impulse from about 30-1 m/ to 90-1 m/s.

Axon Diameter

As the axon diameter increase, the speed of nerve impulses increases as well. This is because a larger axon diminishes the ion-leakage out of the axon. This helps in maintaining the membrane potential and thus favors faster nerve impulses.

Temperature

Temperature cause changes in the rate of diffusion of ions across the neuron membrane. Temperature directly correlates with the transmission of nerve impulses. If the temperature is higher, the rate of diffusion of sodium and potassium ions will be high and axon will become depolarized quickly which will cause a faster nerve impulse conduction.

A nerve impulse is thus an important signal transduction mode for triggering a response in major body parts due to a strong stimulus. Any distraction in this process can have drastic effects on the body.


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Action potential occurs within a neuron when the neuron transmits impulses. During this signal transmission, the membrane potential (the difference in electrical potential between the outside and inside of a cell) of the neuron (specifically the axon) fluctuates with rapid rises and falls. Actions potentials do not occur only in neurons. It occurs in various other excitable cells such as muscle cells, endocrine cells and also in some plant cells. During an action potential, the nerve transmission of impulses takes place along the axon of the neuron up to the synaptic knobs, located at the end of the axon. The prime role of an action potential is to facilitate the communication between cells.

Action potential is normally generated due to a depolarizing current. Due to the opening of K + ion channels for longer periods of time causes the voltage of the action potential to go past -70 mV. But when the Na + ion channels close, this value is brought back to -70mV. These conditions are known as hyperpolarization and repolarization respectively.

Action potential is normally generated due to a depolarizing current. In other terms, a stimulus that generates an action potential causes the resting potential of a neuron to decrease up to 0mV and further down up to a value of -55mV. This is referred to as the threshold value. Unless the neuron reaches the threshold value, an action potential won’t be generated. Similar to resting potentials, action potentials occur due to the crossing of different ions across the membrane of the neuron. Initially, the Na + ion channels are opened up in response to the stimulus. It was mentioned that, during resting potential, the inside of the neuron is more negatively charged and contains more Na + ions outside. Due to the opening of the Na + ion channels during an action potential, more Na + ions will rush into the neuron across the membrane. Due to the + ve charge of sodium ions, the membrane becomes more positively charged and get depolarized.

Figure 02: Action Potential

This depolarization is reversed by the opening of K + ion channels that move a higher number of K + ions out of the neuron. Once the K + ion channels open up, the Na + ion channels close. Due to the opening of K + ion channels for longer periods of time causes the voltage of the action potential to go past -70 mV. This condition is known as hyperpolarization. But when the Na + ion channels close, this value is brought back to -70mV. This is known as repolarization.


Watch the video: Membrane Potential, Equilibrium Potential and Resting Potential, Animation (June 2022).


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