Electrotonic potential

Last updated March 03, 2024

In physiology, electrotonus refers to the passive spread of charge inside a neuron and between cardiac muscle cells or smooth muscle cells. Passive means that voltage-dependent changes in membrane conductance do not contribute. Neurons and other excitable cells produce two types of electrical potential:

Electrotonic potential (or graded potential), a non-propagated local potential, resulting from a local change in ionic conductance (e.g. synaptic or sensory that engenders a local current). When it spreads along a stretch of membrane, it becomes exponentially smaller (decrement).
Action potential, a propagated impulse.

Electrotonic potentials represent changes to the neuron's membrane potential that do not lead to the generation of new current by action potentials.^[1] However, all action potentials are begun by electrotonic potentials depolarizing the membrane above the threshold potential which converts the electrotonic potential into an action potential.^[2] Neurons which are small in relation to their length, such as some neurons in the brain, have only electrotonic potentials (starburst amacrine cells in the retina are believed to have these properties); longer neurons utilize electrotonic potentials to trigger the action potential.

Electrotonic potentials have an amplitude that is usually 5-20 mV and they can last from 1 ms up to several seconds long.^[3] In order to quantify the behavior of electrotonic potentials there are two constants that are commonly used: the membrane time constant τ, and the membrane length constant λ. The membrane time constant measures the amount of time for an electrotonic potential to passively fall to 1/e or 37% of its maximum. A typical value for neurons can be from 1 to 20 ms. The membrane length constant measures how far it takes for an electrotonic potential to fall to 1/e or 37% of its amplitude at the place where it began. Common values for the length constant of dendrites are from .1 to 1 mm.^[2] Electrotonic potentials are conducted faster than action potentials, but attenuate rapidly so are unsuitable for long-distance signaling. The phenomenon was first discovered by Eduard Pflüger.

Summation

The electrotonic potential travels via electrotonic spread, which amounts to attraction of opposite and repulsion of like-charged ions within the cell. Electrotonic potentials can sum spatially or temporally. Spatial summation is the combination of multiple sources of ion influx (multiple channels within a dendrite, or channels within multiple dendrites), whereas temporal summation is a gradual increase in overall charge due to repeated influxes in the same location. Because the ionic charge enters in one location and dissipates to others, losing intensity as it spreads, electrotonic spread is a graded response. It is important to contrast this with the all-or-none law propagation of the action potential down the axon of the neuron.^[2]

EPSPs

Electrotonic potential can either increase the membrane potential with positive charge or decrease it with negative charge. Electrotonic potentials that increase the membrane potential are called excitatory postsynaptic potentials (EPSPs). This is because they depolarize the membrane, increasing the likelihood of an action potential. As they sum together they can depolarize the membrane sufficiently to push it above the threshold potential, which will then cause an action potential to occur. EPSPs are often caused by either Na⁺ or Ca²⁺ coming into the cell.^[2]

IPSPs

Electrotonic potentials which decrease the membrane potential are called inhibitory postsynaptic potentials (IPSPs). They hyperpolarize the membrane and make it harder for a cell to have an action potential. IPSPs are associated with Cl⁻ entering the cell or K⁺ leaving the cell. IPSPs can interact with EPSPs to "cancel out" their effect.^[2]

Information Transfer

Because of the continuously varying nature of the electrotonic potential versus the binary response of the action potential, this creates implications for how much information can be encoded by each respective potential. Electrotonic potentials are able to transfer more information within a given time period than action potentials. This difference in information rates can be up to almost an order of magnitude greater for electrotonic potentials.^[4]^[5]

Cable theory

Cable theory can be useful for understanding how currents flow through the axons of a neuron.^[6] In 1855, Lord Kelvin devised this theory as a way to describe electrical properties of transatlantic telegraph cables.^[7] Almost a century later in 1946, Hodgkin and Rushton discovered cable theory could be applied to neurons as well.^[8] This theory has the neuron approximated as a cable whose radius does not change, and allows it to be represented with the partial differential equation ^[6]^[9]

\tau {\frac {\partial V}{\partial t}}=\lambda ^{2}{\frac {\partial ^{2}V}{\partial x^{2}}}-V

where V(x, t) is the voltage across the membrane at a time t and a position x along the length of the neuron, and where λ and τ are the characteristic length and time scales on which those voltages decay in response to a stimulus. Referring to the circuit diagram on the right, these scales can be determined from the resistances and capacitances per unit length.^[10]

\lambda ={\sqrt {\frac {r_{m}}{r_{\ell }}}}

\tau =\ r_{m}c_{m}\,

From these equations one can understand how properties of a neuron affect the current passing through it. The length constant λ, increases as membrane resistance becomes larger and as the internal resistance becomes smaller, allowing current to travel farther down the neuron. The time constant τ, increases as the resistance and capacitance of the membrane increase, which causes current to travel more slowly through the neuron.^[2]

Ribbon synapses

Ribbon synapses are a type of synapse often found in sensory neurons and are of a unique structure that specially equips them to respond dynamically to inputs from electrotonic potentials. They are so named for an organelle they contain, the synaptic ribbon. This organelle can hold thousands of synaptic vesicles close to the presynaptic membrane, enabling neurotransmitter release that can quickly react to a wide range of changes in the membrane potential.^[11]^[12]

Related Research Articles

A dendrite or dendron is a branched protoplasmic extension of a nerve cell that propagates the electrochemical stimulation received from other neural cells to the cell body, or soma, of the neuron from which the dendrites project. Electrical stimulation is transmitted onto dendrites by upstream neurons via synapses which are located at various points throughout the dendritic tree.

Within a nervous system, a neuron, neurone, or nerve cell is an electrically excitable cell that fires electric signals called action potentials across a neural network. Neurons communicate with other cells via synapses, which are specialized connections that commonly use minute amounts of chemical neurotransmitters to pass the electric signal from the presynaptic neuron to the target cell through the synaptic gap.

Chemical synapses are biological junctions through which neurons' signals can be sent to each other and to non-neuronal cells such as those in muscles or glands. Chemical synapses allow neurons to form circuits within the central nervous system. They are crucial to the biological computations that underlie perception and thought. They allow the nervous system to connect to and control other systems of the body.

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 animal cells, called excitable cells, which include neurons, muscle cells, and in some plant cells. Certain endocrine cells such as pancreatic beta cells, and certain cells of the anterior pituitary gland are also excitable cells.

An inhibitory postsynaptic potential (IPSP) is a kind of synaptic potential that makes a postsynaptic neuron less likely to generate an action potential. The opposite of an inhibitory postsynaptic potential is an excitatory postsynaptic potential (EPSP), which is a synaptic potential that makes a postsynaptic neuron more likely to generate an action potential. IPSPs can take place at all chemical synapses, which use the secretion of neurotransmitters to create cell-to-cell signalling. EPSPs and IPSPs compete with each other at numerous synapses of a neuron. This determines whether an action potential occurring at the presynaptic terminal produces an action potential at the postsynaptic membrane. Some common neurotransmitters involved in IPSPs are GABA and glycine.

In neuroscience, an excitatory postsynaptic potential (EPSP) is a postsynaptic potential that makes the postsynaptic neuron more likely to fire an action potential. This temporary depolarization of postsynaptic membrane potential, caused by the flow of positively charged ions into the postsynaptic cell, is a result of opening ligand-gated ion channels. These are the opposite of inhibitory postsynaptic potentials (IPSPs), which usually result from the flow of negative ions into the cell or positive ions out of the cell. EPSPs can also result from a decrease in outgoing positive charges, while IPSPs are sometimes caused by an increase in positive charge outflow. The flow of ions that causes an EPSP is an excitatory postsynaptic current (EPSC).

Graded potentials are changes in membrane potential that vary according to the size of the stimulus, as opposed to being all-or-none. They include diverse potentials such as receptor potentials, electrotonic potentials, subthreshold membrane potential oscillations, slow-wave potential, pacemaker potentials, and synaptic potentials. The magnitude of a graded potential is determined by the strength of the stimulus. They arise from the summation of the individual actions of ligand-gated ion channel proteins, and decrease over time and space. They do not typically involve voltage-gated sodium and potassium channels, but rather can be produced by neurotransmitters that are released at synapses which activate ligand-gated ion channels. They occur at the postsynaptic dendrite in response to presynaptic neuron firing and release of neurotransmitter, or may occur in skeletal, smooth, or cardiac muscle in response to nerve input. These impulses are incremental and may be excitatory or inhibitory.

An excitatory synapse is a synapse in which an action potential in a presynaptic neuron increases the probability of an action potential occurring in a postsynaptic cell. Neurons form networks through which nerve impulses travels, each neuron often making numerous connections with other cells of neurons. These electrical signals may be excitatory or inhibitory, and, if the total of excitatory influences exceeds that of the inhibitory influences, the neuron will generate a new action potential at its axon hillock, thus transmitting the information to yet another cell.

<span class="mw-page-title-main">Pyramidal cell</span> Projection neurons in the cerebral cortex and hippocampus

Pyramidal cells, or pyramidal neurons, are a type of multipolar neuron found in areas of the brain including the cerebral cortex, the hippocampus, and the amygdala. Pyramidal cells are the primary excitation units of the mammalian prefrontal cortex and the corticospinal tract. Pyramidal neurons are also one of two cell types where the characteristic sign, Negri bodies, are found in post-mortem rabies infection. Pyramidal neurons were first discovered and studied by Santiago Ramón y Cajal. Since then, studies on pyramidal neurons have focused on topics ranging from neuroplasticity to cognition.

The axon hillock is a specialized part of the cell body of a neuron that connects to the axon. It can be identified using light microscopy from its appearance and location in a neuron and from its sparse distribution of Nissl substance.

Postsynaptic potentials are changes in the membrane potential of the postsynaptic terminal of a chemical synapse. Postsynaptic potentials are graded potentials, and should not be confused with action potentials although their function is to initiate or inhibit action potentials. They are caused by the presynaptic neuron releasing neurotransmitters from the terminal bouton at the end of an axon into the synaptic cleft. The neurotransmitters bind to receptors on the postsynaptic terminal, which may be a neuron or a muscle cell in the case of a neuromuscular junction. These are collectively referred to as postsynaptic receptors, since they are on the membrane of the postsynaptic cell.

An apical dendrite is a dendrite that emerges from the apex of a pyramidal cell. Apical dendrites are one of two primary categories of dendrites, and they distinguish the pyramidal cells from spiny stellate cells in the cortices. Pyramidal cells are found in the prefrontal cortex, the hippocampus, the entorhinal cortex, the olfactory cortex, and other areas. Dendrite arbors formed by apical dendrites are the means by which synaptic inputs into a cell are integrated. The apical dendrites in these regions contribute significantly to memory, learning, and sensory associations by modulating the excitatory and inhibitory signals received by the pyramidal cells.

In neuroscience, classical cable theory uses mathematical models to calculate the electric current along passive neurites, particularly the dendrites that receive synaptic inputs at different sites and times. Estimates are made by modeling dendrites and axons as cylinders composed of segments with capacitances $and resistances combined in parallel. The capacitance of a neuronal fiber comes about because electrostatic forces are acting through the very thin lipid bilayer. The resistance in series along the fiber is due to the axoplasm's significant resistance to movement of electric charge.$

<span class="mw-page-title-main">Synaptic potential</span> Potential difference across the postsynaptic membrane

Synaptic potential refers to the potential difference across the postsynaptic membrane that results from the action of neurotransmitters at a neuronal synapse. In other words, it is the “incoming” signal that a neuron receives. There are two forms of synaptic potential: excitatory and inhibitory. The type of potential produced depends on both the postsynaptic receptor, more specifically the changes in conductance of ion channels in the post synaptic membrane, and the nature of the released neurotransmitter. Excitatory post-synaptic potentials (EPSPs) depolarize the membrane and move the potential closer to the threshold for an action potential to be generated. Inhibitory postsynaptic potentials (IPSPs) hyperpolarize the membrane and move the potential farther away from the threshold, decreasing the likelihood of an action potential occurring. The Excitatory Post Synaptic potential is most likely going to be carried out by the neurotransmitters glutamate and acetylcholine, while the Inhibitory post synaptic potential will most likely be carried out by the neurotransmitters gamma-aminobutyric acid (GABA) and glycine. In order to depolarize a neuron enough to cause an action potential, there must be enough EPSPs to both depolarize the postsynaptic membrane from its resting membrane potential to its threshold and counterbalance the concurrent IPSPs that hyperpolarize the membrane. As an example, consider a neuron with a resting membrane potential of -70 mV (millivolts) and a threshold of -50 mV. It will need to be raised 20 mV in order to pass the threshold and fire an action potential. The neuron will account for all the many incoming excitatory and inhibitory signals via summative neural integration, and if the result is an increase of 20 mV or more, an action potential will occur.

Neural backpropagation is the phenomenon in which, after the action potential of a neuron creates a voltage spike down the axon, another impulse is generated from the soma and propagates towards the apical portions of the dendritic arbor or dendrites. In addition to active backpropagation of the action potential, there is also passive electrotonic spread. While there is ample evidence to prove the existence of backpropagating action potentials, the function of such action potentials and the extent to which they invade the most distal dendrites remain highly controversial.

In neurophysiology, a dendritic spike refers to an action potential generated in the dendrite of a neuron. Dendrites are branched extensions of a neuron. They receive electrical signals emitted from projecting neurons and transfer these signals to the cell body, or soma. Dendritic signaling has traditionally been viewed as a passive mode of electrical signaling. Unlike its axon counterpart which can generate signals through action potentials, dendrites were believed to only have the ability to propagate electrical signals by physical means: changes in conductance, length, cross sectional area, etc. However, the existence of dendritic spikes was proposed and demonstrated by W. Alden Spencer, Eric Kandel, Rodolfo Llinás and coworkers in the 1960s and a large body of evidence now makes it clear that dendrites are active neuronal structures. Dendrites contain voltage-gated ion channels giving them the ability to generate action potentials. Dendritic spikes have been recorded in numerous types of neurons in the brain and are thought to have great implications in neuronal communication, memory, and learning. They are one of the major factors in long-term potentiation.

<span class="mw-page-title-main">Summation (neurophysiology)</span>

Summation, which includes both spatial summation and temporal summation, is the process that determines whether or not an action potential will be generated by the combined effects of excitatory and inhibitory signals, both from multiple simultaneous inputs, and from repeated inputs. Depending on the sum total of many individual inputs, summation may or may not reach the threshold voltage to trigger an action potential.

Cellular neuroscience is a branch of neuroscience concerned with the study of neurons at a cellular level. This includes morphology and physiological properties of single neurons. Several techniques such as intracellular recording, patch-clamp, and voltage-clamp technique, pharmacology, confocal imaging, molecular biology, two photon laser scanning microscopy and Ca²⁺ imaging have been used to study activity at the cellular level. Cellular neuroscience examines the various types of neurons, the functions of different neurons, the influence of neurons upon each other, and how neurons work together.

Nonsynaptic plasticity is a form of neuroplasticity that involves modification of ion channel function in the axon, dendrites, and cell body that results in specific changes in the integration of excitatory postsynaptic potentials and inhibitory postsynaptic potentials. Nonsynaptic plasticity is a modification of the intrinsic excitability of the neuron. It interacts with synaptic plasticity, but it is considered a separate entity from synaptic plasticity. Intrinsic modification of the electrical properties of neurons plays a role in many aspects of plasticity from homeostatic plasticity to learning and memory itself. Nonsynaptic plasticity affects synaptic integration, subthreshold propagation, spike generation, and other fundamental mechanisms of neurons at the cellular level. These individual neuronal alterations can result in changes in higher brain function, especially learning and memory. However, as an emerging field in neuroscience, much of the knowledge about nonsynaptic plasticity is uncertain and still requires further investigation to better define its role in brain function and behavior.

Neurotransmitters are released into a synapse in packaged vesicles called quanta. One quantum generates a miniature end plate potential (MEPP) which is the smallest amount of stimulation that one neuron can send to another neuron. Quantal release is the mechanism by which most traditional endogenous neurotransmitters are transmitted throughout the body. The aggregate sum of many MEPPs is an end plate potential (EPP). A normal end plate potential usually causes the postsynaptic neuron to reach its threshold of excitation and elicit an action potential. Electrical synapses do not use quantal neurotransmitter release and instead use gap junctions between neurons to send current flows between neurons. The goal of any synapse is to produce either an excitatory postsynaptic potential (EPSP) or an inhibitory postsynaptic potential (IPSP), which generate or repress the expression, respectively, of an action potential in the postsynaptic neuron. It is estimated that an action potential will trigger the release of approximately 20% of an axon terminal's neurotransmitter load.

References

↑ electrotonic - definition of electrotonic in the Medical dictionary - by the Free Online Medical Dictionary, Thesaurus and Encyclopedia
1 2 3 4 5 6 Sperelakis, Nicholas (2011). Cell Physiology Source Book. Academic Press. pp. 563–578. ISBN 978-0-12-387738-3.
↑ Pauls, John (2014). Clinical Neuroscience. Churchill Livingstone. pp. 71–80. ISBN 978-0-443-10321-6.
↑ Juusola, Mikko (July 1996). "Information processing by graded-potential transmission through tonically active synapses". Trends in Neurosciences. 19 (7): 292–7. doi:10.1016/S0166-2236(96)10028-X. PMID 8799975. S2CID 13180990.
↑ Niven, Jeremy Edward (January 2014). "Consequences of Converting Graded to Action Potentials upon Neural Information Coding and Energy Efficiency". PLOS Computational Biology. 10 (1): e1003439. Bibcode:2014PLSCB..10E3439S. doi: 10.1371/journal.pcbi.1003439 . PMC 3900385 . PMID 24465197. S2CID 15385561.
1 2 Rall, Wilfrid (1998). "Cable Theory for Dendritic Neurons". In Koch, Christof; Segev, Idan (eds.). Methods in Neuronal Modeling: From Ions to Networks. MIT Press. pp. 9–62. ISBN 978-0-262-11231-4.
↑ Kelvin WT (1855). "On the theory of the electric telegraph". Proceedings of the Royal Society. 7: 382–99.
↑ Hodgkin, AL (1946). "The electrical constants of a crustacean nerve fibre". Proceedings of the Royal Society B. 133 (873): 444–79. Bibcode:1946RSPSB.133..444H. doi:10.1098/rspb.1946.0024. PMID 20281590.
↑ Gabbiani, Fabrizio (2017). Mathematics for Neuroscientists. Academic Press. pp. 73–91. ISBN 978-0-12-801895-8.
↑ Purves et al. 2008, pp. 52–53.
↑ Matthews, Gary (January 2005). "Structure and function of ribbon synapses". Trends in Neurosciences. 28 (1): 20–29. doi:10.1016/j.tins.2004.11.009. PMID 15626493. S2CID 16576501.
↑ Lagnado, Leon (August 2013). "Spikes and ribbon synapses in early vision". Trends in Neurosciences. 36 (8): 480–488. doi:10.1016/j.tins.2013.04.006. PMID 23706152. S2CID 28383128.

External links

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[1] trotonic - definition of electrotonic in the Medical dictionary - by the Free Online Medical Dictionary, Thesaurus and Encyclopedia

[:1-2] 1 2 3 4 5 6 Sperelakis, Nicholas (2011). Cell Physiology Source Book. Academic Press. pp. 563–578. ISBN 978-0-12-387738-3.

[3] Pauls, John (2014). Clinical Neuroscience. Churchill Livingstone. pp. 71–80. ISBN 978-0-443-10321-6.

[4] Juusola, Mikko (July 1996). "Information processing by graded-potential transmission through tonically active synapses". Trends in Neurosciences. 19 (7): 292–7. doi:10.1016/S0166-2236(96)10028-X. PMID 8799975. S2CID 13180990.

[5] Niven, Jeremy Edward (January 2014). "Consequences of Converting Graded to Action Potentials upon Neural Information Coding and Energy Efficiency". PLOS Computational Biology. 10 (1): e1003439. Bibcode:2014PLSCB..10E3439S. doi: 10.1371/journal.pcbi.1003439 . PMC 3900385 . PMID 24465197. S2CID 15385561.

[:0-6] 1 2 Rall, Wilfrid (1998). "Cable Theory for Dendritic Neurons". In Koch, Christof; Segev, Idan (eds.). Methods in Neuronal Modeling: From Ions to Networks. MIT Press. pp. 9–62. ISBN 978-0-262-11231-4.

[7] Kelvin WT (1855). "On the theory of the electric telegraph". Proceedings of the Royal Society. 7: 382–99.

[8] Hodgkin, AL (1946). "The electrical constants of a crustacean nerve fibre". Proceedings of the Royal Society B. 133 (873): 444–79. Bibcode:1946RSPSB.133..444H. doi:10.1098/rspb.1946.0024. PMID 20281590.

[9] Gabbiani, Fabrizio (2017). Mathematics for Neuroscientists. Academic Press. pp. 73–91. ISBN 978-0-12-801895-8.

[10] Purves et al. 2008, pp. 52–53.

[11] Matthews, Gary (January 2005). "Structure and function of ribbon synapses". Trends in Neurosciences. 28 (1): 20–29. doi:10.1016/j.tins.2004.11.009. PMID 15626493. S2CID 16576501.

[12] Lagnado, Leon (August 2013). "Spikes and ribbon synapses in early vision". Trends in Neurosciences. 36 (8): 480–488. doi:10.1016/j.tins.2013.04.006. PMID 23706152. S2CID 28383128.

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