Electrical synapse

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Electrical synapse
Gap cell junction-en.svg
Diagram of a gap junction
Identifiers
MeSH D054351
TH H1.00.01.1.02024
FMA 67130
Anatomical terminology

An electrical synapse, or gap junction, is a mechanical and electrically conductive synapse, a functional junction between two neighboring neurons. The synapse is formed at a narrow gap between the pre- and postsynaptic neurons known as a gap junction. At gap junctions, such cells approach within about 3.8 nm of each other, [1] a much shorter distance than the 20- to 40-nanometer distance that separates cells at a chemical synapse. [2] In many[ specify ] animals, electrical synapse-based systems co-exist with chemical synapses.

Contents

Compared to chemical synapses, electrical synapses conduct nerve impulses faster and provide continuous-time bidirectional coupling via linked cytoplasm. [1] [3] [4] [5] As such, the notion of signal directionality across these synapses is not always defined. [5] They are known to produce synchronization of network activity in the brain [6] and can create chaotic network level dynamics [7] [8] . In situations where a signal direction can be defined, they lack gain (unlike chemical synapses)—the signal in the postsynaptic neuron is the same or smaller than that of the originating neuron [ citation needed ]. The fundamental bases for perceiving electrical synapses comes down to the connexons that are located in the gap junction between two neurons. Electrical synapses are often found in neural systems that require the fastest possible response, such as defensive reflexes. An important characteristic of electrical synapses is that they are mostly bidirectional, allowing impulse transmission in either direction. [9] [10]

Structure

Each gap junction (sometimes called a nexus) contains numerous gap junction channels that cross the plasma membranes of both cells. [11] With a lumen diameter of about 1.2 to 2.0 nm, [2] [12] the pore of a gap junction channel is wide enough to allow ions and even medium-size molecules like signaling molecules to flow from one cell to the next, [2] [13] thereby connecting the two cells' cytoplasm. Thus when the membrane potential of one cell changes, ions may move through from one cell to the next, carrying positive charge with them and depolarizing the postsynaptic cell.

Gap junction channels are composed of two hemichannels called connexons in vertebrates, one contributed by each cell at the synapse. [2] [12] [14] Connexons are formed by six 7.5 nm long, four-pass membrane-spanning protein subunits called connexins, which may be identical or slightly different from one another. [12]

An autapse is an electrical (or chemical) synapse formed when the axon of one neuron synapses with its own dendrites.

Effects

They are found in many regions in animal and human body. The simplicity of electrical synapses results in synapses that are fast, but more importantly the bidirectional coupling can produce very complex behaviors at the network level. [15]

The relative speed of electrical synapses also allows for many neurons to fire synchronously. [11] [12] [17] Because of the speed of transmission, electrical synapses are found in escape mechanisms and other processes that require quick responses, such as the response to danger of the sea hare Aplysia , which quickly releases large quantities of ink to obscure enemies' vision. [1]

Normally, current carried by ions could travel in either direction through this type of synapse. [2] However, sometimes the junctions are rectifying synapses, [2] containing voltage-gated ion channels that open in response to depolarization of an axon's plasma membrane, and prevent current from traveling in one of the two directions. [17] Some channels may also close in response to increased calcium (Ca2+
) or hydrogen (H+
) ion concentration, so as not to spread damage from one cell to another. [17]

There is also evidence of synaptic plasticity where the electrical connection established can either be strengthened or weakened as a result of activity, or during changes in the intracellular concentration of magnesium. [18] [19]

Electrical synapses are present throughout the central nervous system and have been studied specifically in the neocortex, hippocampus, thalamic reticular nucleus, locus coeruleus, inferior olivary nucleus, mesencephalic nucleus of the trigeminal nerve, olfactory bulb, retina, and spinal cord of vertebrates. [20] Other examples of functional gap junctions detected in vivo are in the striatum, cerebellum, and suprachiasmatic nucleus. [21] [22]

History

The model of a reticular network of directly interconnected cells was one of the early hypotheses for the organization of the nervous system at the beginning of the 20th century. This reticular hypothesis was considered to conflict directly with the now predominant neuron doctrine , a model in which isolated, individual neurons signal to each other chemically across synaptic gaps. These two models came into sharp contrast at the award ceremony for the 1906 Nobel Prize in Physiology or Medicine, in which the award went jointly to Camillo Golgi, a reticularist and widely recognized cell biologist, and Santiago Ramón y Cajal, the champion of the neuron doctrine and the father of modern neuroscience. Golgi delivered his Nobel lecture first, in part detailing evidence for a reticular model of the nervous system. Ramón y Cajal then took the podium and refuted Golgi's conclusions in his lecture. Modern understanding of the coexistence of chemical and electrical synapses, however, suggests that both models are physiologically significant; it could be said that the Nobel committee acted with great foresight in awarding the Prize jointly.

There was substantial debate on whether the transmission of information between neurons was chemical or electrical in the first decades of the twentieth century, but chemical synaptic transmission was seen as the only answer after Otto Loewi's demonstration of chemical communication between neurons and heart muscle. Thus, the discovery of electrical communication was surprising.

Electrical synapses were first demonstrated between escape-related giant neurons in crayfish in the late 1950s, [23] and were later found in vertebrates. [9]

See also

Related Research Articles

<span class="mw-page-title-main">Dendrite</span> Small projection on a neuron that receives signals

A dendrite or dendron is a branched cytoplasmic process that extends from 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.

<span class="mw-page-title-main">Neuron</span> Electrically excitable cell found in the nervous system of animals

A neuron, neurone, or nerve cell is an excitable cell that fires electric signals called action potentials across a neural network in the nervous system. 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.

<span class="mw-page-title-main">Chemical synapse</span> Biological junctions through which neurons signals can be sent

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.

<span class="mw-page-title-main">Gap junction</span> Cell-cell junction composed of innexins or connexins

Gap junctions are membrane channels between adjacent cells that allow the direct exchange of cytoplasmic substances. Substances exchanged include small molecules, substrates, and metabolites.

<span class="mw-page-title-main">Synaptic plasticity</span> Ability of a synapse to strengthen or weaken over time according to its activity

In neuroscience, synaptic plasticity is the ability of synapses to strengthen or weaken over time, in response to increases or decreases in their activity. Since memories are postulated to be represented by vastly interconnected neural circuits in the brain, synaptic plasticity is one of the important neurochemical foundations of learning and memory.

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.

<span class="mw-page-title-main">Excitatory postsynaptic potential</span> Process causing temporary increase in postsynaptic potential

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).

In neurophysiology, long-term depression (LTD) is an activity-dependent reduction in the efficacy of neuronal synapses lasting hours or longer following a long patterned stimulus. LTD occurs in many areas of the CNS with varying mechanisms depending upon brain region and developmental progress.

<span class="mw-page-title-main">Excitatory synapse</span> Sort of synapse

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.

Synaptogenesis is the formation of synapses between neurons in the nervous system. Although it occurs throughout a healthy person's lifespan, an explosion of synapse formation occurs during early brain development, known as exuberant synaptogenesis. Synaptogenesis is particularly important during an individual's critical period, during which there is a certain degree of synaptic pruning due to competition for neural growth factors by neurons and synapses. Processes that are not used, or inhibited during their critical period will fail to develop normally later on in life.

<span class="mw-page-title-main">Neurotransmission</span> Impulse transmission between neurons

Neurotransmission is the process by which signaling molecules called neurotransmitters are released by the axon terminal of a neuron, and bind to and react with the receptors on the dendrites of another neuron a short distance away. A similar process occurs in retrograde neurotransmission, where the dendrites of the postsynaptic neuron release retrograde neurotransmitters that signal through receptors that are located on the axon terminal of the presynaptic neuron, mainly at GABAergic and glutamatergic synapses.

<span class="mw-page-title-main">Synapse</span> Structure connecting neurons in the nervous system

In the nervous system, a synapse is a structure that permits a neuron to pass an electrical or chemical signal to another neuron or to the target effector cell. Synapses can be chemical or electrical. In case of electrical synapses, neurons are coupled bidirectionally in continuous-time to each other and are known to produce synchronous network activity in the brain but can result in much more complicated network level dynamics like chaos. As such, signal directionality cannot always be defined across electrical synapses.

<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.

<span class="mw-page-title-main">Dendritic spike</span> Action potential generated in the dendrite of a neuron

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">Axon terminal</span> Nerve fiber part

Axon terminals are distal terminations of the branches of an axon. An axon, also called a nerve fiber, is a long, slender projection of a nerve cell that conducts electrical impulses called action potentials away from the neuron's cell body to transmit those impulses to other neurons, muscle cells, or glands. Most presynaptic terminals in the central nervous system are formed along the axons, not at their ends.

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.

<span class="mw-page-title-main">Nonsynaptic plasticity</span> Form of neuroplasticity

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.

Anoxic depolarization is a progressive and uncontrollable depolarization of neurons during stroke or brain ischemia in which there is an inadequate supply of blood to the brain. Anoxic depolarization is induced by the loss of neuronal selective membrane permeability and the ion gradients across the membrane that are needed to support neuronal activity. Normally, the Na+/K+-ATPase pump maintains the transmembrane gradients of K+ and Na+ ions, but with anoxic brain injury, the supply of energy to drive this pump is lost. The hallmarks of anoxic depolarization are increased concentrations of extracellular K+ ions, intracellular Na+ and Ca2+ ions, and extracellular glutamate and aspartate. Glutamate and aspartate are normally present as the brain's primary excitatory neurotransmitters, but high concentrations activate a number of downstream apoptotic and necrotic pathways. This results in neuronal dysfunction and brain death.

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.

<span class="mw-page-title-main">Synaptic stabilization</span> Modifying synaptic strength via cell adhesion molecules

Synaptic stabilization is crucial in the developing and adult nervous systems and is considered a result of the late phase of long-term potentiation (LTP). The mechanism involves strengthening and maintaining active synapses through increased expression of cytoskeletal and extracellular matrix elements and postsynaptic scaffold proteins, while pruning less active ones. For example, cell adhesion molecules (CAMs) play a large role in synaptic maintenance and stabilization. Gerald Edelman discovered CAMs and studied their function during development, which showed CAMs are required for cell migration and the formation of the entire nervous system. In the adult nervous system, CAMs play an integral role in synaptic plasticity relating to learning and memory.

References

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  2. 1 2 3 4 5 6 Hormuzdi SG, Filippov MA, Mitropoulou G, Monyer H, Bruzzone R (March 2004). "Electrical synapses: a dynamic signaling system that shapes the activity of neuronal networks". Biochim. Biophys. Acta. 1662 (1–2): 113–37. doi: 10.1016/j.bbamem.2003.10.023 . PMID   15033583.
  3. ↑ Purves, Dale; Williams, Stephen Mark, eds. (2004). Neuroscience (3rd ed.). Sunderland, Mass: Sinauer Associates. ISBN   978-0-87893-915-2.
  4. ↑ Bennett, M. V. L. (1966). "PHYSIOLOGY OF ELECTROTONIC JUNCTIONS*". Annals of the New York Academy of Sciences. 137 (2): 509–539. doi:10.1111/j.1749-6632.1966.tb50178.x. ISSN   0077-8923.
  5. 1 2 Connors, Barry W.; Long, Michael A. (2004-07-21). "ELECTRICAL SYNAPSES IN THE MAMMALIAN BRAIN". Annual Review of Neuroscience. 27 (1): 393–418. doi:10.1146/annurev.neuro.26.041002.131128. ISSN   0147-006X.
  6. ↑ Bennett, Michael V.L; Zukin, R.Suzanne (2004). "Electrical Coupling and Neuronal Synchronization in the Mammalian Brain". Neuron. 41 (4): 495–511. doi:10.1016/S0896-6273(04)00043-1.
  7. ↑ Makarenko, Vladimir; Llinás, Rodolfo (1998-12-22). "Experimentally determined chaotic phase synchronization in a neuronal system". Proceedings of the National Academy of Sciences. 95 (26): 15747–15752. doi:10.1073/pnas.95.26.15747. ISSN   0027-8424. PMC   28115 . PMID   9861041.
  8. ↑ Korn, Henri; Faure, Philippe (2003-09-01). "Is there chaos in the brain? II. Experimental evidence and related models". Comptes Rendus. Biologies. 326 (9): 787–840. doi:10.1016/j.crvi.2003.09.011. ISSN   1768-3238.
  9. 1 2 Purves, Dale; George J. Augustine; David Fitzpatrick; William C. Hall; Anthony-Samuel LaMantia; James O. McNamara & Leonard E. White (2008). Neuroscience (4th ed.). Sinauer Associates. pp. 85–88. ISBN   978-0-87893-697-7.
  10. ↑ Purves, Dale; George J. Augustine; David Fitzpatrick; William C. Hall; Anthony-Samuel LaMantia; Richard D. Mooney; Leonard E. White & Michael L. Platt (2018). Neuroscience (6th ed.). Oxford University Press. pp. 86–87. ISBN   978-1605353807.
  11. 1 2 Gibson JR, Beierlein M, Connors BW (January 2005). "Functional properties of electrical synapses between inhibitory interneurons of neocortical layer 4". J. Neurophysiol. 93 (1): 467–80. doi:10.1152/jn.00520.2004. PMID   15317837.
  12. 1 2 3 4 5 Bennett MV, Zukin RS (February 2004). "Electrical coupling and neuronal synchronization in the Mammalian brain". Neuron. 41 (4): 495–511. doi: 10.1016/S0896-6273(04)00043-1 . PMID   14980200. S2CID   18566176.
  13. ↑ Kandel, Schwartz & Jessell 2000 , pp. 178–180
  14. ↑ Kandel, Schwartz & Jessell 2000 , p. 178
  15. ↑ Rydin Gorjão, Leonardo; Saha, Arindam; Ansmann, Gerrit; Feudel, Ulrike; Lehnertz, Klaus (2018-10-01). "Complexity and irreducibility of dynamics on networks of networks". Chaos: An Interdisciplinary Journal of Nonlinear Science. 28 (10). doi:10.1063/1.5039483. ISSN   1054-1500.
  16. ↑ Dr. John O'Brien || Faculty Biography || The Department of Ophthalmology and Visual Science at the University of Texas Medical School at Houston
  17. 1 2 3 Kandel, Schwartz & Jessell 2000 , p. 180
  18. ↑ Palacios-Prado, Nicolas; et al. (Mar 2013). "Intracellular magnesium-dependent modulation of gap junction channels formed by neuronal connexin36". Journal of Neuroscience. 33 (11): 4741–53. doi:10.1523/JNEUROSCI.2825-12.2013. PMC   3635812 . PMID   23486946.
  19. ↑ Activity-Dependent; Synapses, Electrical; Haas, Julie S.; et al. (2011). "Activity-dependent long-term depression of electrical synapses". Science. 334 (6054): 389–93. Bibcode:2011Sci...334..389H. doi:10.1126/science.1207502. PMC   10921920 . PMID   22021860. S2CID   35398480.
  20. ↑ Electrical synapses in the mammalian brain, Connors & Long, "Annu Rev Neurosci" 2004;27:393-418
  21. ↑ Eugenin, Eliseo A.; Basilio, Daniel; Sáez, Juan C.; Orellana, Juan A.; Raine, Cedric S.; Bukauskas, Feliksas; Bennett, Michael V. L.; Berman, Joan W. (2012-09-01). "The role of gap junction channels during physiologic and pathologic conditions of the human central nervous system". Journal of Neuroimmune Pharmacology. 7 (3): 499–518. doi:10.1007/s11481-012-9352-5. ISSN   1557-1904. PMC   3638201 . PMID   22438035.
  22. ↑ Pereda, Alberto E.; Curti, Sebastian; Hoge, Gregory; Cachope, Roger; Flores, Carmen E.; Rash, John E. (2013-01-01). "Gap junction-mediated electrical transmission: regulatory mechanisms and plasticity". Biochimica et Biophysica Acta (BBA) - Biomembranes. 1828 (1): 134–146. doi:10.1016/j.bbamem.2012.05.026. ISSN   0006-3002. PMC   3437247 . PMID   22659675.
  23. ↑ Pappas, George D.; Bennett, Michael V. L. (1966). "Specialized junctions involved in electrical transmission between neurons". Annals of the New York Academy of Sciences. 137 (2): 495–508. doi:10.1111/j.1749-6632.1966.tb50177.x. ISSN   0077-8923.

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