Encyclopedia of Animal Cognition and Behavior

Living Edition
| Editors: Jennifer Vonk, Todd Shackelford

Action Potentials

  • Natalia PrietoEmail author
  • Joseph Wrobleski
Living reference work entry

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DOI: https://doi.org/10.1007/978-3-319-47829-6_1268-2
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Keywords

Terminal Buttons Scaling Potential Extracellular Electrical Activity Positive Equilibrium Potential Axon Hillock 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Synonyms

Definition

An action potential is a brief event that occurs when there is a change in the membrane potential, or electrical activity, of a neuron.

Introduction

Action potentials play an integral part of communication between neurons and are involved in many processes within the central nervous system, neuromuscular junctions, and cardiac functions. They occur in response to a stimulus, such as sensory input or neurotransmitters, usually through the dendrites of the neuron. These stimuli cause small excitations in the dendrites or cell body called graded potentials. Graded potentials are summated and must be strong enough to trigger the impulse. At rest, the inside of a neuron is negative relative to the outside. Once it is stimulated, the intracellular environment becomes positive relative to the outside of the cell, thus allowing ion channels to open and sodium (Na+) to move into the axon. Most neurons have a protein called myelin that surrounds segments of the axon and insulates them from extracellular electrical activity. Small sections that remain unmyelinated are referred to as nodes of Ranvier. These nodes contain many ion channels that help the action potential regenerate as it travels down the axon. Myelin allows for the action potential to quickly travel from node to node, as it promotes low resistance for the conduction of positive ions. This action of jumping from node to node is called saltatory conduction. Once the action potential travels down the axon, there is a positive spike in the membrane potential that causes a release of neurotransmitters into the synapse through the neuron’s terminal buttons.

All-or-None Principle

A neuron is connected to thousands of other neurons; therefore it can receive numerous stimuli at one point in time. The strength of the stimuli does not affect the amplitude, or intensity, of an action potential. In addition, an action potential is only generated if there is sufficient stimulation. These properties make up the all-or-none principle. In other words, an action potential will have the same intensity of firing regardless of the intensity of a stimulus. While the strength of the stimulus does not affect the intensity of the action potential, it does affect the frequency of firing (Barnett and Larkman 2007).

Measurement of an Action Potential

An action potential can be measured by recording the electrical potential of the cell membrane using electrodes. Electrical activity is most commonly measured using two points, one as a reference and another to record changes in potential, relative to the reference point. The extracellular environment is used as the reference point for recording electrical changes in a neuron. When the recording electrode is inserted into the axon, a negative potential is measured. This indicates that, at rest, the inside of the neuron is more negative than the extracellular environment.

Each ion involved in the action potential has a concentration gradient due to the permeability of the membrane. The potential for each ion can be measured by the Nernst equation: \( {E}_i=\frac{RT}{zF}\mathit{\ln}\frac{\left[C\right]o}{\left[C\right]i} \). In this equation E i indicates the equilibrium of a single ion, R is the Universal Gas constant, T is temperature, z is the charge of the ion, F is Faraday’s constant, C o is the concentration of the ion outside the cell, and C i is the concentration of the ion inside the cell (Hille 2001). Outside of the cell, there is a high concentration of sodium, calcium, and other ions, while the inside has a high concentration of potassium (K+). Each of these ions has an equilibrium potential (E i ) as a result of the concentration gradient. Na+ has a positive equilibrium potential (E Na.) of about +55 mV. K+ has a negative equilibrium potential (E K ) of about −75 mV (Barnett and Larkman 2007). The resting potential of the cell is at about −60 mV. As ions move across the membrane, the membrane voltage (V m ) and permeability change. In order to calculate the membrane potential of a cell, the Goldman equation is used: \( {V}_m=58\log \frac{P_k{\left[K\right]}_2+{P}_{\mathrm{Na}}{\left[\mathrm{Na}\right]}_2+{P}_{\mathrm{Cl}}{\left[\mathrm{Cl}\right]}_1}{P_k{\left[K\right]}_1+{P}_{\mathrm{Na}}{\left[\mathrm{Na}\right]}_1+{P}_{\mathrm{Cl}}{\left[\mathrm{Cl}\right]}_2} \), where P indicates the permeability of the cell (Purves et al. 2001a).

During an action potential (Fig. 1), the Na+ channels open and V m increases or depolarizes, toward E Na. As more Na+ rush into the cell, a positive feedback loop occurs. Na+ increases V m , which opens more voltage-gated ion channels, allowing more Na+ into the cell, further increasing V m toward E Na. The loop repeats until all the Na+ channels open and the cell reaches the peak voltage of the action potential, meaning the concentration of Na+ is equal on both sides of the membrane. This point is known as the absolute refractory period. During this period, no more Na+ can enter the cell to create another action potential. The high V m then inactivates the Na+ channels and opens the voltage-gated K+ channels. As this occurs, K+ rush out of the cell and V m decreases or repolarizes, toward E K+. During this period, action potentials are unlikely but possible only in response to strong stimuli. This is known as the relative refractory period. Since E K is lower than −60 mV, V m falls under the resting potential resulting in hyperpolarization (Purves et al. 2001a). The cell then repolarizes back to resting potential via the sodium-potassium pump.
Fig. 1

Stages of action potential. Membrane potential starts at rest at −70 mV. Once threshold is reached at −45 mV, the membrane potential depolarizes toward the Na+ potential at +55 mV. At this point, known as the absolute refractory period, another action potential cannot occur because no more Na+ can enter the cell. The membrane then repolarizes to the equilibrium potential of potassium at −75 mV. During this stage, the relative refractory period, only strong stimuli can elicit another action potential. The membrane then goes back to resting potential by action of the sodium-potassium pump

Sodium-Potassium Pump

A neuron maintains a resting potential around −60 mV due to an electrochemical gradient created by the active transport of the sodium-potassium pump (Na+/K+ pump). This transporter works by pumping three Na+ ions out and two K+ ions into the cell. At rest, the extracellular environment has a higher concentration of Na+, while the intracellular environment has a higher concentration of K+. The Na+/K+ pump requires ATP as energy because it moves the ions against their concentration gradients. This action results in a deficit of positive ions inside the cell making it negative relative to the extracellular environment (Glitsch 2001).

Initiation

There are three steps to the occurrence of an action potential: initiation, propagation, and termination. Initiation of the action potential begins with a stimulus that causes ion channels to open, usually on the dendrites or cell body. A stimulus can be excitatory or inhibitory. When a neurotransmitter binds to a receptor that increases the probability for depolarization, it is called an excitatory postsynaptic potential (EPSP). When a neurotransmitter binds to a receptor to increase the chance for hyperpolarization, it is called an inhibitory postsynaptic potential (IPSP) (Purves et al. 2001b). EPSPs and IPSPs alter the permeability of the membrane by affecting the ion channels (Krnjevik 1987). Positive or negative ions enter the cell body and work their way along the membrane toward the axon hillock, where they are collected and summated. This movement across the membrane causes small variations in electrical potential of the cell, known as graded potentials. The graded potentials must sufficiently depolarize the cell and bring the membrane potential to a threshold, usually −40 mV, in order for an action potential to occur. Once the membrane potential reaches the threshold, the axon hillock experiences a reversal in charge, where it becomes positive relative to the outside of the cell (Palmer and Stuart 2006).

Propagation

Once the action potential is initiated, the positive charge in the axon hillock is propagated to the adjacent, unmyelinated segment of the axon (Palmer and Stuart 2006). As the flow of positive ions moves into adjacent segments, Na+ and K+ voltage-gated ion channels are activated. Na+ channels open first, allowing the positive ions to rush into the cell (Fig. 2b). Once the inside of the axon becomes positive, the channels deactivate via a ball and chain mechanism in which a ball blocks the channel, preventing further Na+ from entering the cell (Fig. 2c). This systematic deactivation is called the refractory period and prevents the action potential from moving backward. Furthermore, the negative electrostatic charge in the following segment pulls the positive ions forward. As the Na+ channels inactivate, voltage-gated K+ channels open and allow K+ to move out of the cell, following their concentration gradient (Fig. 2d). This is known as repolarization. The K+ channels are slow to deactivate and bring the segment below resting potential, hyperpolarizing it (Fig. 2e) (Barnett and Larkman 2007). The action of the Na+/K+ pump brings each segment back to resting potential from the hyperpolarized state.
Fig. 2

Propagation of action potential down the first and second segment of an axon. (a) Neuron membrane at rest with no stimulus. (b) Sodium channels on membrane open as a response to the positive charge of the axon hillock, and Na+ rushes into the cell as reversal of charge occurs. (c) Sodium channels in the first segment inactivate. Na+ are pulled down the myelinated portion of the axon to the second segment, and the sodium channels open. (d) Potassium channels open in the first segment, and K+ rush out of the cell. In the second segment, sodium channels inactivate and Na+ are pulled down the myelinated axon to the third segment (not shown). (e) Potassium channels close, sodium channels close, and the cell returns to resting potential in the first segment. Potassium channels open, and K+ rush out of the cell in the second segment. This process continues down the segments of the axons

Termination

Chemical

Termination takes place when neurotransmitters are released into the synapse through the neuron’s terminal buttons. When an action potential reaches these buttons, the positive charge opens voltage-gated calcium (Ca++) channels. Ca++ rush into the cell following their concentration gradient. The Ca++ bind to proteins that attach neurotransmitter-containing vesicles to the membrane of the terminal button. A conformational change occurs in the proteins so that they pull and fuse the vesicles to the membrane, allowing neurotransmitters to be released into the synaptic cleft. This process is known as exocytosis (Llinas et al. 1981).

Neuromuscular

Termination of an action potential can also have different physiological effects. In a neuromuscular junction, the action potential of a motor neuron will elicit the contraction of a muscle fiber. In this case, the neurotransmitter released by the presynaptic cell is acetylcholine, or Ach. The muscle cell contains sodium and calcium ion channels that have an Ach receptor. When it binds, these channels open causing the ions to rush into the cell. Inside the cell, the calcium binds to receptors in the sarcoplasmic reticulum, which contains a large supply of calcium ions. This action causes the release of the ions which spread from cell to cell and fiber to fiber causing the muscle to contract (Lodish et al. 2000).

Cross-References

References

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© Springer International Publishing AG 2018

Authors and Affiliations

  1. 1.Hofstra UniversityHempsteadUSA

Section editors and affiliations

  • Oskar Pineno
    • 1
  1. 1.Hofstra UniversityLong IslandUSA