what role to the nodes of ranvier play in the conduction of an action potential?

The Nervous System and Nervous Tissue

The Action Potential

OpenStaxCollege

Learning Objectives

By the stop of this department, you volition exist able to:

• Draw the components of the membrane that establish the resting membrane potential
• Describe the changes that occur to the membrane that result in the action potential

The functions of the nervous system—sensation, integration, and response—depend on the functions of the neurons underlying these pathways. To understand how neurons are able to communicate, it is necessary to depict the role of an excitable membrane in generating these signals. The basis of this communication is the activeness potential, which demonstrates how changes in the membrane can found a signal. Looking at the way these signals piece of work in more variable circumstances involves a look at graded potentials, which will be covered in the adjacent section.

Electrically Agile Cell Membranes

Most cells in the torso make use of charged particles, ions, to build upwards a charge beyond the jail cell membrane. Previously, this was shown to be a part of how muscle cells work. For skeletal muscles to contract, based on excitation–contraction coupling, requires input from a neuron. Both of the cells brand use of the cell membrane to regulate ion movement between the extracellular fluid and cytosol.

Every bit you learned in the chapter on cells, the cell membrane is primarily responsible for regulating what can cross the membrane and what stays on only i side. The jail cell membrane is a phospholipid bilayer, so only substances that tin pass directly through the hydrophobic cadre can diffuse through unaided. Charged particles, which are hydrophilic by definition, cannot pass through the cell membrane without aid ([link]). Transmembrane proteins, specifically channel proteins, make this possible. Several passive ship channels, every bit well as agile send pumps, are necessary to generate a transmembrane potential and an activity potential. Of special interest is the carrier protein referred to every bit the sodium/potassium pump that moves sodium ions (Na⁺) out of a jail cell and potassium ions (G⁺) into a prison cell, thus regulating ion concentration on both sides of the cell membrane.

Cell Membrane and Transmembrane Proteins

The cell membrane is composed of a phospholipid bilayer and has many transmembrane proteins, including different types of channel proteins that serve equally ion channels.

The sodium/potassium pump requires energy in the form of adenosine triphosphate (ATP), so it is also referred to every bit an ATPase. Every bit was explained in the cell chapter, the concentration of Na⁺ is higher outside the cell than inside, and the concentration of One thousand⁺ is higher inside the cell than outside. That means that this pump is moving the ions against the concentration gradients for sodium and potassium, which is why it requires free energy. In fact, the pump basically maintains those concentration gradients.

Ion channels are pores that allow specific charged particles to cross the membrane in response to an existing concentration slope. Proteins are capable of spanning the cell membrane, including its hydrophobic core, and tin interact with the accuse of ions because of the varied properties of amino acids plant inside specific domains or regions of the protein channel. Hydrophobic amino acids are constitute in the domains that are apposed to the hydrocarbon tails of the phospholipids. Hydrophilic amino acids are exposed to the fluid environments of the extracellular fluid and cytosol. Additionally, the ions will interact with the hydrophilic amino acids, which volition be selective for the charge of the ion. Channels for cations (positive ions) will have negatively charged side chains in the pore. Channels for anions (negative ions) will have positively charged side bondage in the pore. This is called electrochemical exclusion, meaning that the aqueduct pore is accuse-specific.

Ion channels can too be specified by the diameter of the pore. The distance between the amino acids will be specific for the bore of the ion when it dissociates from the water molecules surrounding it. Because of the surrounding water molecules, larger pores are non ideal for smaller ions because the water molecules will interact, past hydrogen bonds, more readily than the amino acrid side chains. This is chosen size exclusion. Some ion channels are selective for charge just not necessarily for size, and thus are called a nonspecific channel. These nonspecific channels allow cations—particularly Na⁺, K⁺, and Ca²⁺—to cantankerous the membrane, just exclude anions.

Ion channels do not ever freely allow ions to diffuse across the membrane. Some are opened by sure events, pregnant the channels are gated. So another way that channels can exist categorized is on the ground of how they are gated. Although these classes of ion channels are institute primarily in the cells of nervous or muscular tissue, they likewise can be constitute in the cells of epithelial and connective tissues.

A ligand-gated aqueduct opens because a signaling molecule, a ligand, binds to the extracellular region of the aqueduct. This blazon of channel is also known equally an ionotropic receptor because when the ligand, known as a neurotransmitter in the nervous organization, binds to the protein, ions cantankerous the membrane changing its charge ([link]).

Ligand-Gated Channels

When the ligand, in this case the neurotransmitter acetylcholine, binds to a specific location on the extracellular surface of the aqueduct protein, the pore opens to let select ions through. The ions, in this example, are cations of sodium, calcium, and potassium.

A mechanically gated channel opens because of a physical distortion of the cell membrane. Many channels associated with the sense of touch (somatosensation) are mechanically gated. For case, equally pressure is applied to the skin, these channels open and allow ions to enter the cell. Similar to this blazon of channel would be the channel that opens on the basis of temperature changes, as in testing the water in the shower ([link]).

Mechanically Gated Channels

When a mechanical change occurs in the surrounding tissue, such every bit pressure or touch, the channel is physically opened. Thermoreceptors work on a similar principle. When the local tissue temperature changes, the poly peptide reacts by physically opening the channel.

A voltage-gated channel is a channel that responds to changes in the electrical properties of the membrane in which information technology is embedded. Normally, the inner portion of the membrane is at a negative voltage. When that voltage becomes less negative, the aqueduct begins to allow ions to cantankerous the membrane ([link]).

Voltage-Gated Channels

Voltage-gated channels open up when the transmembrane voltage changes around them. Amino acids in the structure of the protein are sensitive to charge and crusade the pore to open to the selected ion.

A leakage channel is randomly gated, pregnant that information technology opens and closes at random, hence the reference to leaking. There is no actual effect that opens the aqueduct; instead, it has an intrinsic rate of switching between the open and closed states. Leakage channels contribute to the resting transmembrane voltage of the excitable membrane ([link]).

Leakage Channels

In certain situations, ions demand to movement across the membrane randomly. The particular electrical properties of certain cells are modified by the presence of this type of channel.

The Membrane Potential

The electrical state of the prison cell membrane tin can take several variations. These are all variations in the membrane potential. A potential is a distribution of charge across the cell membrane, measured in millivolts (mV). The standard is to compare the inside of the cell relative to the outside, so the membrane potential is a value representing the charge on the intracellular side of the membrane based on the outside being zero, relatively speaking ([link]).

Measuring Charge beyond a Membrane with a Voltmeter

A recording electrode is inserted into the jail cell and a reference electrode is exterior the prison cell. By comparing the charge measured past these two electrodes, the transmembrane voltage is determined. It is conventional to express that value for the cytosol relative to the outside.

The concentration of ions in extracellular and intracellular fluids is largely balanced, with a cyberspace neutral charge. However, a slight difference in charge occurs right at the membrane surface, both internally and externally. It is the divergence in this very express region that has all the ability in neurons (and muscle cells) to generate electrical signals, including action potentials.

Before these electrical signals can exist described, the resting land of the membrane must be explained. When the cell is at rest, and the ion channels are airtight (except for leakage channels which randomly open), ions are distributed across the membrane in a very predictable way. The concentration of Na⁺ outside the cell is ten times greater than the concentration within. Also, the concentration of K⁺ inside the cell is greater than outside. The cytosol contains a high concentration of anions, in the class of phosphate ions and negatively charged proteins. Large anions are a component of the inner jail cell membrane, including specialized phospholipids and proteins associated with the inner leaflet of the membrane (leaflet is a term used for ane side of the lipid bilayer membrane). The negative charge is localized in the large anions.

With the ions distributed across the membrane at these concentrations, the difference in charge is measured at -lxx mV, the value described as the resting membrane potential. The exact value measured for the resting membrane potential varies between cells, but -seventy mV is virtually normally used equally this value. This voltage would actually be much lower except for the contributions of some of import proteins in the membrane. Leakage channels let Na⁺ to slowly move into the jail cell or Thousand⁺ to slowly motility out, and the Na⁺/K⁺ pump restores them. This may announced to be a waste of energy, but each has a role in maintaining the membrane potential.

The Action Potential

Resting membrane potential describes the steady state of the cell, which is a dynamic process that is counterbalanced by ion leakage and ion pumping. Without any outside influence, it will not change. To get an electrical signal started, the membrane potential has to change.

This starts with a channel opening for Na⁺ in the membrane. Because the concentration of Na⁺ is higher exterior the jail cell than within the cell past a factor of x, ions will rush into the jail cell that are driven largely past the concentration gradient. Considering sodium is a positively charged ion, it will change the relative voltage immediately within the cell relative to immediately exterior. The resting potential is the state of the membrane at a voltage of -70 mV, and so the sodium cation entering the cell will crusade it to become less negative. This is known as depolarization, pregnant the membrane potential moves toward nix.

The concentration gradient for Na⁺ is so strong that it will go on to enter the cell even after the membrane potential has go zero, so that the voltage immediately around the pore begins to become positive. The electrical slope also plays a role, as negative proteins below the membrane attract the sodium ion. The membrane potential will reach +xxx mV by the time sodium has entered the cell.

As the membrane potential reaches +thirty mV, other voltage-gated channels are opening in the membrane. These channels are specific for the potassium ion. A concentration gradient acts on K⁺, as well. Equally K⁺ starts to leave the cell, taking a positive charge with it, the membrane potential begins to move back toward its resting voltage. This is called repolarization, meaning that the membrane voltage moves back toward the -seventy mV value of the resting membrane potential.

Repolarization returns the membrane potential to the -70 mV value that indicates the resting potential, but information technology really overshoots that value. Potassium ions accomplish equilibrium when the membrane voltage is below -70 mV, so a menses of hyperpolarization occurs while the Yard⁺ channels are open. Those K⁺ channels are slightly delayed in closing, accounting for this short overshoot.

What has been described here is the activeness potential, which is presented as a graph of voltage over time in [link]. Information technology is the electrical signal that nervous tissue generates for communication. The change in the membrane voltage from -70 mV at residuum to +thirty mV at the end of depolarization is a 100-mV modify. That can as well be written as a 0.1-5 alter. To put that value in perspective, think nearly a battery. An AA bombardment that yous might find in a television remote has a voltage of 1.5 V, or a 9-V battery (the rectangular bombardment with two posts on ane finish) is, obviously, 9 V. The change seen in the activeness potential is one or ii orders of magnitude less than the charge in these batteries. In fact, the membrane potential tin be described as a bombardment. A charge is stored across the membrane that can be released under the correct weather. A bombardment in your remote has stored a charge that is "released" when y'all push a button.

Graph of Activeness Potential

Plotting voltage measured across the cell membrane confronting fourth dimension, the activity potential begins with depolarization, followed by repolarization, which goes past the resting potential into hyperpolarization, and finally the membrane returns to rest.

What happens across the membrane of an electrically active prison cell is a dynamic procedure that is hard to visualize with static images or through text descriptions. View this animation to acquire more about this procedure. What is the deviation between the driving force for Na⁺ and 1000⁺? And what is similar about the movement of these two ions?

The question is, at present, what initiates the action potential? The description higher up conveniently glosses over that indicate. But it is vital to agreement what is happening. The membrane potential will stay at the resting voltage until something changes. The description higher up just says that a Na⁺ channel opens. Now, to say "a channel opens" does not hateful that one individual transmembrane protein changes. Instead, information technology ways that one kind of channel opens. At that place are a few different types of channels that let Na⁺ to cross the membrane. A ligand-gated Na⁺ channel will open when a neurotransmitter binds to it and a mechanically gated Na⁺ channel will open up when a physical stimulus affects a sensory receptor (similar pressure level applied to the pare compresses a touch receptor). Whether it is a neurotransmitter binding to its receptor poly peptide or a sensory stimulus activating a sensory receptor jail cell, some stimulus gets the process started. Sodium starts to enter the cell and the membrane becomes less negative.

A third blazon of channel that is an important part of depolarization in the activeness potential is the voltage-gated Na⁺ channel. The channels that start depolarizing the membrane because of a stimulus aid the prison cell to depolarize from -70 mV to -55 mV. Once the membrane reaches that voltage, the voltage-gated Na⁺ channels open. This is what is known as the threshold. Any depolarization that does not change the membrane potential to -55 mV or higher will not attain threshold and thus will not result in an action potential. Also, any stimulus that depolarizes the membrane to -55 mV or beyond will cause a large number of channels to open and an action potential will be initiated.

Considering of the threshold, the activity potential tin can be likened to a digital result—it either happens or it does not. If the threshold is not reached, then no action potential occurs. If depolarization reaches -55 mV, then the action potential continues and runs all the way to +xxx mV, at which 1000⁺ causes repolarization, including the hyperpolarizing overshoot. Besides, those changes are the same for every activity potential, which means that once the threshold is reached, the verbal same thing happens. A stronger stimulus, which might depolarize the membrane well past threshold, will non brand a "bigger" activeness potential. Action potentials are "all or none." Either the membrane reaches the threshold and everything occurs every bit described above, or the membrane does not accomplish the threshold and nothing else happens. All action potentials peak at the same voltage (+30 mV), then ane action potential is not bigger than some other. Stronger stimuli will initiate multiple activeness potentials more quickly, but the individual signals are not bigger. Thus, for example, you will not feel a greater sensation of pain, or have a stronger muscle contraction, considering of the size of the action potential because they are not different sizes.

As we take seen, the depolarization and repolarization of an activeness potential are dependent on two types of channels (the voltage-gated Na⁺ channel and the voltage-gated K⁺ channel). The voltage-gated Na⁺ channel actually has two gates. One is the activation gate, which opens when the membrane potential crosses -55 mV. The other gate is the inactivation gate, which closes after a specific period of fourth dimension—on the order of a fraction of a millisecond. When a cell is at residual, the activation gate is airtight and the inactivation gate is open. However, when the threshold is reached, the activation gate opens, assuasive Na⁺ to blitz into the cell. Timed with the elevation of depolarization, the inactivation gate closes. During repolarization, no more sodium can enter the jail cell. When the membrane potential passes -55 mV again, the activation gate closes. After that, the inactivation gate re-opens, making the channel ready to offset the whole procedure over over again.

The voltage-gated K⁺ channel has merely one gate, which is sensitive to a membrane voltage of -50 mV. Notwithstanding, information technology does not open as rapidly as the voltage-gated Na⁺ channel does. It might take a fraction of a millisecond for the aqueduct to open one time that voltage has been reached. The timing of this coincides exactly with when the Na⁺ menstruum peaks, so voltage-gated K⁺ channels open just equally the voltage-gated Na⁺ channels are being inactivated. As the membrane potential repolarizes and the voltage passes -50 mV again, the channel closes—again, with a little filibuster. Potassium continues to get out the jail cell for a short while and the membrane potential becomes more negative, resulting in the hyperpolarizing overshoot. Then the channel closes again and the membrane can render to the resting potential because of the ongoing action of the non-gated channels and the Na⁺/Thousand⁺ pump.

All of this takes place within approximately 2 milliseconds ([link]). While an action potential is in progress, another 1 cannot exist initiated. That issue is referred to as the refractory period. At that place are two phases of the refractory flow: the absolute refractory period and the relative refractory period. During the absolute phase, another activeness potential will not kickoff. This is because of the inactivation gate of the voltage-gated Na⁺ aqueduct. One time that channel is back to its resting conformation (less than -55 mV), a new action potential could be started, but only by a stronger stimulus than the one that initiated the electric current action potential. This is because of the flow of Grand⁺ out of the jail cell. Because that ion is rushing out, whatever Na⁺ that tries to enter will not depolarize the cell, merely will only go on the cell from hyperpolarizing.

Stages of an Action Potential

Plotting voltage measured beyond the cell membrane confronting time, the events of the action potential can be related to specific changes in the membrane voltage. (1) At rest, the membrane voltage is -70 mV. (2) The membrane begins to depolarize when an external stimulus is applied. (3) The membrane voltage begins a rapid rise toward +thirty mV. (4) The membrane voltage starts to return to a negative value. (5) Repolarization continues past the resting membrane voltage, resulting in hyperpolarization. (half-dozen) The membrane voltage returns to the resting value shortly after hyperpolarization.

Propagation of the Action Potential

The activity potential is initiated at the starting time of the axon, at what is called the initial segment. There is a high density of voltage-gated Na⁺ channels so that rapid depolarization can take place here. Going downwards the length of the axon, the action potential is propagated because more voltage-gated Na⁺ channels are opened equally the depolarization spreads. This spreading occurs because Na⁺ enters through the channel and moves along the inside of the jail cell membrane. Every bit the Na⁺ moves, or flows, a brusk altitude forth the cell membrane, its positive charge depolarizes a piddling more of the prison cell membrane. As that depolarization spreads, new voltage-gated Na⁺ channels open and more ions rush into the prison cell, spreading the depolarization a little farther.

Because voltage-gated Na⁺ channels are inactivated at the peak of the depolarization, they cannot exist opened once again for a brief time—the absolute refractory menses. Considering of this, depolarization spreading back toward previously opened channels has no outcome. The action potential must propagate toward the axon terminals; equally a event, the polarity of the neuron is maintained, as mentioned above.

Propagation, every bit described higher up, applies to unmyelinated axons. When myelination is present, the action potential propagates differently. Sodium ions that enter the cell at the initial segment outset to spread along the length of the axon segment, but there are no voltage-gated Na⁺ channels until the first node of Ranvier. Because there is not constant opening of these channels along the axon segment, the depolarization spreads at an optimal speed. The distance between nodes is the optimal altitude to keep the membrane however depolarized above threshold at the next node. As Na⁺ spreads along the inside of the membrane of the axon segment, the charge starts to dissipate. If the node were whatsoever farther downwardly the axon, that depolarization would have fallen off too much for voltage-gated Na⁺ channels to be activated at the next node of Ranvier. If the nodes were any closer together, the speed of propagation would exist slower.

Propagation along an unmyelinated axon is referred to as continuous conduction; along the length of a myelinated axon, it is saltatory conduction. Continuous conduction is slow because there are always voltage-gated Na⁺ channels opening, and more and more Na⁺ is rushing into the cell. Saltatory conduction is faster considering the action potential basically jumps from one node to the side by side (saltare = "to leap"), and the new influx of Na⁺ renews the depolarized membrane. Along with the myelination of the axon, the diameter of the axon can influence the speed of conduction. Much as water runs faster in a wide river than in a narrow creek, Na⁺-based depolarization spreads faster downward a wide axon than down a narrow one. This concept is known as resistance and is by and large true for electrical wires or plumbing, only as information technology is true for axons, although the specific conditions are unlike at the scales of electrons or ions versus water in a river.

Homeostatic Imbalances

Potassium Concentration
Glial cells, especially astrocytes, are responsible for maintaining the chemic surroundings of the CNS tissue. The concentrations of ions in the extracellular fluid are the footing for how the membrane potential is established and changes in electrochemical signaling. If the balance of ions is upset, drastic outcomes are possible.

Usually the concentration of K⁺ is higher within the neuron than exterior. Subsequently the repolarizing stage of the activity potential, G⁺ leakage channels and the Na⁺/Chiliad⁺ pump ensure that the ions return to their original locations. Post-obit a stroke or other ischemic event, extracellular Chiliad⁺ levels are elevated. The astrocytes in the area are equipped to articulate excess G⁺ to assist the pump. But when the level is far out of balance, the furnishings tin exist irreversible.

Astrocytes can become reactive in cases such as these, which impairs their ability to maintain the local chemic environs. The glial cells enlarge and their processes keen. They lose their K⁺ buffering ability and the role of the pump is affected, or even reversed. One of the early signs of cell affliction is this "leaking" of sodium ions into the body cells. This sodium/potassium imbalance negatively affects the internal chemistry of cells, preventing them from operation commonly.

Visit this site to run across a virtual neurophysiology lab, and to observe electrophysiological processes in the nervous system, where scientists directly measure out the electrical signals produced by neurons. Ofttimes, the activeness potentials occur so chop-chop that watching a screen to see them occur is non helpful. A speaker is powered by the signals recorded from a neuron and information technology "pops" each time the neuron fires an action potential. These action potentials are firing so fast that it sounds like static on the radio. Electrophysiologists can recognize the patterns within that static to understand what is happening. Why is the leech model used for measuring the electrical activity of neurons instead of using humans?

Chapter Review

The nervous system is characterized by electric signals that are sent from 1 surface area to another. Whether those areas are close or very far apart, the signal must travel along an axon. The basis of the electrical signal is the controlled distribution of ions across the membrane. Transmembrane ion channels regulate when ions can motion in or out of the cell, and then that a precise signal is generated. This betoken is the activeness potential which has a very feature shape based on voltage changes across the membrane in a given time flow.

The membrane is normally at rest with established Na⁺ and G⁺ concentrations on either side. A stimulus will start the depolarization of the membrane, and voltage-gated channels will outcome in further depolarization followed by repolarization of the membrane. A slight overshoot of hyperpolarization marks the end of the action potential. While an action potential is in progress, some other cannot exist generated under the same weather condition. While the voltage-gated Na⁺ channel is inactivated, admittedly no activeness potentials tin can be generated. Once that channel has returned to its resting state, a new action potential is possible, but information technology must be started by a relatively stronger stimulus to overcome the Thousand⁺ leaving the prison cell.

The action potential travels down the axon every bit voltage-gated ion channels are opened by the spreading depolarization. In unmyelinated axons, this happens in a continuous fashion because at that place are voltage-gated channels throughout the membrane. In myelinated axons, propagation is described as saltatory because voltage-gated channels are simply plant at the nodes of Ranvier and the electric events seem to "leap" from one node to the next. Saltatory conduction is faster than continuous conduction, meaning that myelinated axons propagate their signals faster. The bore of the axon also makes a difference equally ions diffusing within the cell have less resistance in a wider infinite.

Interactive Link Questions

What happens across the membrane of an electrically agile cell is a dynamic procedure that is hard to visualize with static images or through text descriptions. View this animation to really understand the process. What is the departure between the driving force for Na⁺ and K⁺? And what is similar about the move of these two ions?

Sodium is moving into the jail cell because of the immense concentration gradient, whereas potassium is moving out because of the depolarization that sodium causes. However, they both move down their respective gradients, toward equilibrium.

Visit this site to come across a virtual neurophysiology lab, and to observe electrophysiological processes in the nervous organisation, where scientists direct measure out the electric signals produced by neurons. Often, the action potentials occur so rapidly that watching a screen to see them occur is not helpful. A speaker is powered by the signals recorded from a neuron and information technology "pops" each fourth dimension the neuron fires an action potential. These action potentials are firing so fast that it sounds like static on the radio. Electrophysiologists tin recognize the patterns within that static to sympathize what is happening. Why is the leech model used for measuring the electrical action of neurons instead of using humans?

The backdrop of electrophysiology are common to all animals, so using the leech is an easier, more than humane approach to studying the backdrop of these cells. There are differences between the nervous systems of invertebrates (such as a leech) and vertebrates, but non for the sake of what these experiments written report.

Review Questions

What ion enters a neuron causing depolarization of the cell membrane?

1. sodium
2. chloride
3. potassium
4. phosphate

A

Voltage-gated Na⁺ channels open up upon reaching what state?

1. resting potential
2. threshold
3. repolarization
4. overshoot

B

What does a ligand-gated aqueduct crave in order to open?

1. increase in concentration of Na⁺ ions
2. binding of a neurotransmitter
3. increase in concentration of K⁺ ions
4. depolarization of the membrane

B

What does a mechanically gated channel respond to?

1. physical stimulus
2. chemic stimulus
3. increase in resistance
4. decrease in resistance

A

Which of the following voltages would most likely be measured during the relative refractory period?

1. +30 mV
2. 0 mV
3. -45 mV
4. -80 mv

D

Which of the following is probably going to propagate an activity potential fastest?

1. a thin, unmyelinated axon
2. a thin, myelinated axon
3. a thick, unmyelinated axon
4. a thick, myelinated axon

D

Disquisitional Thinking Questions

What does it mean for an activeness potential to be an "all or none" event?

The jail cell membrane must attain threshold before voltage-gated Na⁺ channels open. If threshold is not reached, those channels exercise not open, and the depolarizing stage of the activity potential does non occur, the jail cell membrane will merely go dorsum to its resting state.

The conscious perception of hurting is ofttimes delayed because of the time information technology takes for the sensations to reach the cognitive cortex. Why would this exist the instance based on propagation of the axon potential?

Axons of pain sensing sensory neurons are sparse and unmyelinated so that it takes longer for that sensation to achieve the brain than other sensations.

Glossary

accented refractory menses

time during an action period when some other action potential cannot be generated because the voltage-gated Na⁺ channel is inactivated

activation gate

function of the voltage-gated Na⁺ channel that opens when the membrane voltage reaches threshold

continuous conduction

slow propagation of an action potential along an unmyelinated axon owing to voltage-gated Na⁺ channels located along the entire length of the prison cell membrane

depolarization

change in a prison cell membrane potential from residue toward zero

electrochemical exclusion

principle of selectively assuasive ions through a channel on the footing of their charge

excitable membrane

cell membrane that regulates the motility of ions so that an electric indicate can be generated

gated

property of a channel that determines how information technology opens nether specific weather condition, such as voltage alter or physical deformation

inactivation gate

part of a voltage-gated Na⁺ channel that closes when the membrane potential reaches +30 mV

ionotropic receptor

neurotransmitter receptor that acts equally an ion channel gate, and opens by the binding of the neurotransmitter

leakage channel

ion channel that opens randomly and is not gated to a specific outcome, also known as a non-gated channel

ligand-gated channels

another name for an ionotropic receptor for which a neurotransmitter is the ligand

mechanically gated channel

ion channel that opens when a concrete consequence directly affects the structure of the protein

membrane potential

distribution of charge beyond the cell membrane, based on the charges of ions

nonspecific aqueduct

channel that is not specific to one ion over another, such every bit a nonspecific cation aqueduct that allows any positively charged ion across the membrane

refractory period

time afterwards the initiation of an action potential when another action potential cannot be generated

relative refractory period

time during the refractory period when a new activeness potential tin just be initiated past a stronger stimulus than the electric current action potential because voltage-gated K⁺ channels are not airtight

repolarization

return of the membrane potential to its normally negative voltage at the end of the action potential

resistance

property of an axon that relates to the ability of particles to diffuse through the cytoplasm; this is inversely proportional to the fiber diameter

resting membrane potential

the difference in voltage measured beyond a cell membrane nether steady-state weather condition, typically -70 mV

saltatory conduction

quick propagation of the activity potential along a myelinated axon owing to voltage-gated Na⁺ channels beingness present only at the nodes of Ranvier

size exclusion

principle of selectively assuasive ions through a channel on the basis of their relative size

voltage-gated channel

ion aqueduct that opens because of a change in the charge distributed across the membrane where it is located

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Source: http://pressbooks-dev.oer.hawaii.edu/anatomyandphysiology/chapter/the-action-potential/

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