Beatrice Lang
Action potentials are nerve signals or nerve impulses that neurons use to communicate information throughout the body. They are rapid electrical impulses that travel the length of the axon and cause the release of neurotransmitters into the synapse. The conduction velocity of these electrical signals can be influenced by the diameter of the axon. However, the transmission of these signals from neurons to their target tissues also involves chemical processes. This is because the nerve impulse is transmitted from the axon ending to the target tissue by chemical substances called neurotransmitters. These neurotransmitters can be excitatory or inhibitory, stimulating or hindering the target cell from firing its own action potential.
| Characteristics | Values |
|---|---|
| Definition | A series of quick changes in voltage across a cell membrane |
| Occurrence | Neurons, muscle cells, some plant cells, and certain endocrine cells |
| Initiation | Depolarization, e.g. injection of sodium cations into the cell |
| Phases | Depolarization, overshoot, repolarization |
| Additional states | Hypopolarization, hyperpolarization |
| Electrical cause | Stimulus with certain value expressed in millivolts |
| Chemical cause | Synapses converting electrical signals into chemical signals |
| Synapses | Electrical, Chemical, or both |
| Electrical synapses | Faster transmission, used in escape reflexes, retina of vertebrates, and the heart |
| Chemical synapses | Slower transmission due to diffusion of neurotransmitters |
| Ion channels | Voltage-gated sodium and potassium channels |
| Ion movement | Based on extracellular fluid concentrations, electrostatic effects, and chemical environment |
| Myelination | Increases propagation speed and enables saltatory conduction |
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What You'll Learn
Action potentials are electrical events
During depolarization, the membrane potential rapidly increases to the threshold potential, typically around −50 to −55 mV, opening voltage-gated sodium channels and causing an influx of sodium ions (Na+). This influx further increases the positivity inside the cell, leading to the overshoot phase, where the membrane potential exceeds the electrochemical equilibrium for sodium of approximately +60 mV. Subsequently, the sodium permeability decreases, and potassium ions (K+) start to leave the cell during the repolarization phase. The membrane potential returns to its resting value of approximately −70 mV, but it temporarily overshoots this value due to a delay in the closing of potassium channels.
The electrical nature of action potentials was first identified by Emil du Bois-Reymond in 1843, who observed a diminution in resting currents when stimulating muscle and nerve preparations. Action potentials are essential for cell-to-cell communication, particularly in neurons, where they enable the propagation of signals along the neuron's axon toward synaptic boutons. At the synapse, the electrical signal of the action potential is converted into a chemical signal through the release of neurotransmitters, which can excite or inhibit the target cell.
The speed of action potential propagation is influenced by factors such as the diameter of the axon and the presence of myelin, which increases propagation speed by enhancing the thickness of the fiber. Saltatory conduction, where the action potential jumps from one node to the next, also contributes to faster propagation, particularly in myelinated axons. Inhibitors of ion channels are valuable research tools, allowing scientists to selectively "turn off" specific channels and study their roles in action potential formation.
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Ion channels and their inhibitors
Ion channels are pore-forming membrane proteins that play a crucial role in the transmission of electrical signals in neurons and other excitable cells. These channels selectively allow ions to pass through the plasma membrane, contributing to the cell's membrane potential. The movement of ions across the membrane is driven by both electrical forces and chemical forces. The electrical force arises from the attraction of opposite charges and the repulsion of similar charges, while the chemical force, or force of diffusion, is determined by the concentration gradient of ions across the membrane.
Ligand-gated ion channels (LGICs) are a class of ion channels that are activated by the binding of specific ligands or neurotransmitters. These channels are responsible for fast synaptic transmission in the nervous system and play a crucial role in cell signaling. Examples of LGICs include nicotinic acetylcholine (nAch) receptors, GABAA receptors, and glutamate receptors. Inhibitors of LGICs, such as curare and nitrous oxide, have important medical applications but can also be toxic. For instance, curare is used to relax muscles during surgery, while nitrous oxide, an anesthetic, acts by modulating a broad range of ligand-gated ion channels.
Voltage-gated ion channels (VGICs), on the other hand, are responsive to changes in the membrane potential. These channels open or close in response to alterations in the voltage across the membrane, allowing or blocking the flow of ions. Sodium and potassium channels are examples of VGICs that play a crucial role in the generation of action potentials in neurons and muscle cells. Sodium channels contribute to the depolarization phase, while potassium channels are involved in the repolarization phase. Inhibitors of VGICs, such as certain anticonvulsants, act by blocking sodium or calcium channels, reducing the release of excitatory neurotransmitters.
Ion channel inhibitors have been explored as potential treatments for various diseases, including cancer and neurological disorders. For example, in cancer immunotherapy, blocking potassium channels has been shown to enhance the effectiveness of immune checkpoint inhibitors by improving the activity of effector T cells. Calcium channel blockers have also been investigated as possible anticancer drugs due to their ability to disrupt Ca2+ signaling in tumor cells. Additionally, drugs targeting GABA receptors, such as acamprosate, have been used in the management of neurological disorders like alcohol dependence and anxiety.
In summary, ion channels are essential for the transmission of electrical signals in excitable cells, and their inhibitors serve important research and medical purposes. By selectively blocking or activating specific ion channels, scientists and medical professionals can gain a better understanding of their functions and develop targeted treatments for various diseases, including cancer and neurological disorders. However, it is crucial to approach ion channel inhibitors with caution, as they can also have toxic effects, especially when targeting vital processes such as neuromuscular transmission.
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Synapses and neurotransmitters
An action potential is a rapid electrical impulse that neurons use to communicate information throughout the body. It is a sudden, fast, and transitory change of the resting membrane potential. The conduction velocity of action potentials was first measured in 1850 by Hermann von Helmholtz.
Neurons transmit information to one another through electrical impulses and chemical messengers. The process of neurons passing information to each other is called neurotransmission. Signals are passed from one neuron to another at junctions called synapses. In most circuits, a synapse includes the end of an axon, the dendrite of an adjacent neuron, and a space between the two called the synaptic cleft.
The synaptic cleft is wide enough that electrical signals cannot directly impact the next neuron. Instead, chemical signals called neurotransmitters cross the synapse. Neurotransmitters are released from special pouches clustered near the cell membrane called synaptic vesicles. When an action potential arrives at the axon terminal, the voltage change triggers ion channels in the membrane to open, allowing calcium ions to flow into the cell. When the calcium ions bind to packages of neurotransmitter molecules, the vesicles fuse with the cell membrane at the axon terminal and empty their contents into the synaptic cleft.
The molecules are then taken up by membrane receptors on the post-synaptic, or neighboring, cell. These receptors are proteins located either on the surface of or within a cell that can bind to signaling molecules known as ligands. When the receptors bind the transmitter, they open, altering the voltage across the postsynaptic membrane. Unbound transmitters are degraded, recycled, or diffused out of the cleft.
There are two types of receptors on the postsynaptic membrane. In an ionotropic receptor, a neurotransmitter binds directly to part of an ion channel. The channel is normally closed, but when the neurotransmitter attaches, the receptor protein changes shape, widening the tunnel in the center of the ion channel so that ions can move through.
Excitatory neurons make neurotransmitters that open ion channels that depolarize the dendrite's membrane, while inhibitory neurons make neurotransmitters that hyperpolarize it. The brain's most common excitatory neurotransmitter is glutamate, and its most common inhibitory neurotransmitter is gamma-aminobutyric acid (GABA).
Some synapses directly connect the presynaptic and postsynaptic cells together, allowing ionic currents to directly stimulate the postsynaptic cell. These electrical synapses are used whenever a fast response and coordination of timing are crucial, such as in escape reflexes, the retina of vertebrates, and the heart.
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Electrostatic and chemical forces
Action potentials are nerve signals or nerve impulses that neurons use to communicate information throughout the body. They are rapid electrical impulses that occur in excitable cells such as animal cells like neurons and muscle cells, as well as some plant cells. Action potentials also occur in certain endocrine cells such as pancreatic beta cells and certain cells of the anterior pituitary gland.
The action potential is caused by a combination of electrostatic and chemical forces. Electrostatic force is the force of attraction between two objects with opposite charges and the repulsive force between two objects of similar charges. For instance, a positive sodium ion (Na+) would be attracted to a negative intracellular voltage. The chemical force, or force of diffusion, is defined by the relative extracellular and intracellular concentrations of the ion. The equilibrium potential is the voltage at which these two forces cancel each other out, resulting in no net flux of the ion.
During an action potential, the membrane potential of a specific cell rapidly rises and falls, causing adjacent locations to undergo depolarization as well. This depolarization is often caused by the injection of extra sodium cations into the cell from sources such as chemical synapses, sensory neurons, or pacemaker potentials. The sodium channels are subject to fast inactivation, where the channel pore gets blocked by the linker region between domain III and IV, preventing ion movement.
The conduction velocity of action potentials is influenced by the diameter of the axon and the presence of myelin, which increases the propagation speed by increasing the thickness of the fiber. Saltatory conduction is faster than continuous conduction as the action potential jumps from one node to the next, and the new influx of Na+ renews the depolarized membrane.
Overall, the interplay of electrostatic and chemical forces is crucial in driving the action potential and facilitating communication between neurons.
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Action potential phases
An action potential is a rapid sequence of changes in the voltage across a cell membrane. It is a sudden, fast, transitory, and propagating change of the resting membrane potential. An action potential has three phases: depolarization, overshoot, and repolarization. There are two more states of the membrane potential related to the action potential: hypopolarization, which precedes depolarization, and hyperpolarization, which follows repolarization.
Hypopolarization is the initial increase of the membrane potential to the value of the threshold potential. The threshold potential opens voltage-gated sodium channels and causes a large influx of sodium ions. This phase is called depolarization. During depolarization, the inside of the cell becomes more and more electropositive, until the potential gets closer to the electrochemical equilibrium for sodium of about +60 mV. This phase of extreme positivity is the overshoot phase.
After the overshoot, the sodium permeability suddenly decreases due to the closing of its channels. The overshoot value of the cell potential opens voltage-gated potassium channels, causing a large potassium efflux and decreasing the cell's electropositivity. This phase is the repolarization phase, whose purpose is to restore the resting membrane potential. Repolarization always leads first to hyperpolarization, a state in which the membrane potential is more negative than the default membrane potential.
The speed of action potential propagation along myelinated axons is increased throughout development as myelin thickens and the distance between nodes of Ranvier lengthens. Myelin acts as an insulator that prevents current from leaving the axon, increasing the speed of action potential conduction. In demyelinating diseases like multiple sclerosis, action potential conduction slows because current leaks from previously insulated axon areas.
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Frequently asked questions
From an electrical standpoint, an action potential is caused by a stimulus with a certain value expressed in millivolts [mV]. Not all stimuli can cause an action potential. The stimulus must have a sufficient electrical value that will reduce the negativity of the nerve cell to the threshold of the action potential.
An action potential occurs when the membrane potential of a specific cell rapidly rises and falls. This depolarization then causes adjacent locations to similarly depolarize. Action potentials occur in several types of excitable cells, which include animal cells like neurons and muscle cells, as well as some plant cells.
Synapses are the junction between the nerve cell and its target tissue. In humans, synapses are chemical, meaning that the nerve impulse is transmitted from the axon ending to the target tissue by neurotransmitters (ligands). When an action potential reaches the presynaptic terminal, it causes neurotransmitters to be released from the neuron into the synaptic cleft.
