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| + | In the [[nervous system]], a '''synapse''' is a structure that permits a [[neuron]] (or nerve cell) to pass an electrical or chemical signal to another [[Cell (biology)|cell]] (neural or otherwise).<ref>{{cite book |last1=Schacter |first1=Daniel L. |authorlink1=Daniel Schacter |last2=Gilbert |first2=Daniel T. |authorlink2=Daniel Gilbert (psychologist) |last3=Wegner |first3=Daniel M. |authorlink3=Daniel Wegner |title=Psychology |edition=2nd |year=2011 |publisher=Worth Publishers |location=New York |page=80 |isbn=978-1-4292-3719-2 |oclc=696604625 |lccn=2010940234}}</ref> [[Santiago Ramón y Cajal]] proposed that neurons are not continuous throughout the body, yet still communicate with each other, an idea known as the [[neuron doctrine]].<ref>{{cite book |last1=Elias |first1=Lorin J. |last2=Saucier |first2=Deborah M. |title=Neuropsychology: Clinical and Experimental Foundations |year=2006 |publisher=[[Pearson Education|Pearson/Allyn & Bacon]] |location=Boston |isbn=978-0-20534361-4 |oclc=61131869 |lccn=2005051341}}</ref> |
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| − | [[Image:SynapseIllustration2.svg|thumb|350px|Illustration of the major elements in a prototypical '''synapse'''. Synapses allow [[neuron|nerve cells]] to communicate with one another through [[axon]]s and [[dendrite]]s, converting [[action potential|electrical impulses]] into [[neurotransmitter|chemical]] signals.]] |
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| + | The word "synapse" (from [[Ancient Greek|Greek]] ''synapsis'' "conjunction," from ''synaptein'' "to clasp," from ''syn''- "together" and ''haptein'' "to fasten") was introduced in 1897 by English physiologist [[Michael Foster (physiologist)|Michael Foster]] at the suggestion of English classical scholar Arthur Woollgar Verrall.<ref>{{cite web|title=synapse|url=http://www.etymonline.com/index.php?term=synapse|publisher=[[Online Etymology Dictionary]] |accessdate=2013-10-01}}</ref><ref>{{cite journal |last=Tansey |first=E.M. |year=1997 |title=Not committing barbarisms: Sherrington and the synapse, 1897 |journal=[[Brain Research Bulletin]] |volume=44 |issue=3 |pages=211–212 |location=Amsterdam |publisher=[[Elsevier]] |pmid=9323432 |doi=10.1016/S0361-9230(97)00312-2 |accessdate=2013-10-01 |url=http://www.ncbi.nlm.nih.gov/pubmed/9323432 |quote=The word synapse first appeared in 1897, in the seventh edition of Michael Foster's ''Textbook of Physiology''.}}</ref> |
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| − | '''Chemical synapses''' are specialized junctions through which the cells of the [[nervous system]] signal to each other and to non-neuronal cells such as those in [[muscle]]s or [[gland]]s. Chemical synapses allow the [[neuron]]s of the [[central nervous system]] to form interconnected neural circuits. They are thus crucial to the biological computations that underlie perception and thought. They provide the means through which the nervous system connects to and controls the other systems of the body. A chemical synapse between a motor neuron and a muscle cell is called a [[neuromuscular junction]]; this type of synapse is well-understood. |
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| + | Synapses are essential to neuronal function: neurons are cells that are specialized to pass signals to individual target cells, and synapses are the means by which they do so. At a synapse, the [[plasma membrane]] of the signal-passing neuron (the ''presynaptic'' neuron) comes into close apposition with the membrane of the target (''postsynaptic'') cell. Both the presynaptic and postsynaptic sites contain extensive arrays of [[Molecular biology|molecular machinery]] that link the two membranes together and carry out the signaling process. In many synapses, the presynaptic part is located on an [[axon]], but some presynaptic sites are located on a [[dendrite]] or [[soma (biology)|soma]]. [[Astrocyte]]s also exchange information with the synaptic neurons, responding to synaptic activity and, in turn, regulating [[neurotransmission]].<ref>{{cite journal |last1=Perea |first1=G. |last2=Navarrete |first2=M. |last3=Araque |first3=A. |year=2009 |month=August |title=Tripartite synapses: astrocytes process and control synaptic information |journal=[[Trends (journals)|Trends in Neurosciences]] |volume=32 |issue=8 |pages=421–431 |location=Cambridge, MA |publisher=[[Cell Press]] |pmid=19615761 |doi=10.1016/j.tins.2009.05.001 |accessdate=2013-10-01 |url=http://www.ncbi.nlm.nih.gov/pubmed/19615761}}</ref> |
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| − | Young children have about 10<sup>16</sup> synapses (10 quadrillion). This number declines with age, stabilizing by adulthood. Estimates for adults vary from 10<sup>15</sup> to 5 × 10<sup>15</sup> (1-5 quadrillion) synapses. |
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| + | There are two fundamentally different types of synapses: |
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| − | The word "synapse" comes from "synaptein", which Sir [[Charles Scott Sherrington]] and his colleagues coined from the Greek "syn-" ("together") and "haptein" ("to clasp"). Chemical synapses are not the only type of biological synapse: [[electrical synapse|electrical]] and [[immunological synapse]]s exist as well. Without a qualifier, however, "synapse" commonly refers to a chemical synapse. |
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| + | *In a [[chemical synapse]], electrical activity in the presynaptic neuron is converted (via the activation of [[Voltage-dependent calcium channel|voltage-gated calcium channels]]) into the release of a chemical called a [[neurotransmitter]] that binds to [[neurotransmitter receptor|receptors]] located in the postsynaptic cell, usually embedded in the plasma membrane. The neurotransmitter may initiate an electrical response or a secondary messenger pathway that may either excite or inhibit the postsynaptic neuron. Because of the complexity of receptor [[signal transduction]], chemical synapses can have complex effects on the postsynaptic cell. |
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| − | The signal across a synapse may be regarded as ''neurocrine'', analogous to the types of signaling of the [[endocrine system]] (endocrine, paracrine and autocrine). |
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| + | *In an [[electrical synapse]], the presynaptic and postsynaptic cell membranes are connected by special channels called [[gap junction]]s that are capable of passing electric current, causing voltage changes in the presynaptic cell to induce voltage changes in the postsynaptic cell. The main advantage of an electrical synapse is the rapid transfer of signals from one cell to the next.<ref>{{cite book |last=Silverthorn |first=Dee Unglaub |others=Illustration coordinator William C. Ober; illustrations by Claire W. Garrison; clinical consultant Andrew C. Silverthorn; contributions by Bruce R. Johnson |title=Human Physiology: An Integrated Approach |edition=4th |year=2007 |publisher=[[Pearson Education|Pearson/Benjamin Cummings]] |location=San Francisco |page=271 |isbn=978-0-8053-6851-2 |oclc=62742632 |lccn=2005056517}}</ref> |
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| − | ==Anatomy== |
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| − | [[Image:Complete neuron cell diagram.svg|thumb|301px|left|a diagram of a nerve cell showing the different places where a synapse could occur]] |
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| − | At an archetypal chemical synapse, such as those found at [[dendritic spine]]s, a mushroom-shaped bud projects from each of two cells toward each other. At this interface, the [[biological membrane|membrane]]s of the two cells flank each other across a slender gap, the narrowness of which enables signaling molecules known as [[neurotransmitter]]s to pass rapidly from one cell to the other by [[diffusion]]. This gap, which is about 20 nm wide, is known as the [[synaptic cleft]]. |
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| + | Synaptic communication is distinct from [[ephaptic coupling]], in which communication between neurons occurs via indirect electric fields. |
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| − | Synapses are asymmetric both in structure and in how they operate. Only the so-called presynaptic neuron secretes the neurotransmitter, which binds to [[transmembrane receptor|receptor]]s facing into the synapse from the postsynaptic cell. The presynaptic nerve terminal (also called the synaptic button, bouton, or knob) generally buds from the tip of an [[axon]], while the post-synaptic target surface typically appears on a [[dendrite]], a cell body, or another part of a cell. The parts of synapses where neurotransmitters are released are called the active zones.<ref name="KandelPrin"> |
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| − | Kandel et al., 2000, p. 182 |
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| − | </ref> At active zones, the membranes of the two adjacent cells are held in close contact by [[cell adhesion]] proteins. Immediately behind the postsynaptic membrane is an elaborate complex of interlinked proteins called the [[postsynaptic density]]. Proteins in the postsynaptic density serve a myriad of roles, from anchoring and trafficking neurotransmitter receptors into the plasma membrane, to anchoring various proteins which modulate the activity of the receptors. The postsynaptic cell need not be a neuron, and can also be a [[gland]] or [[muscle]] cell. |
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| + | ==Synaptic polarization== |
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| − | == Signaling across chemical synapses == |
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| + | The function of neurons depends upon [[cell polarity|cellular polarization]]. The distinctive structure of nerve cells allows [[action potential]]s to travel directionally (from dendrites to axons), and for these signals to then be received and carried on by post-synaptic neurons or received by effector cells. Nerve cells have long been used as models for cellular polarization, and of particular interest are the mechanisms underlying the polarized localization of synaptic molecules. [[Phosphatidylinositol 4,5-bisphosphate|PIP2]] signalling regulated by [[Inositol monophosphatase|IMPase]] plays an integral role in synaptic polarity. |
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| ⚫ | |||
| − | The release of a neurotransmitter is triggered by the arrival of a nerve impulse (or [[action potential]]) and occurs through an unusually rapid process of cellular secretion, also known as [[exocytosis]]: Within the presynaptic nerve terminal, [[vesicle (biology)|vesicle]]s containing neurotransmitter sit "docked" and ready at the synaptic membrane. The arriving action potential produces an influx of [[second messenger|calcium ions]] through [[Voltage-dependent calcium channel| voltage-dependent, calcium-selective ion channels]] at the down stroke of the action potential (tail current).<ref name="Llinás81"> |
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| − | {{ |
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| − | cite journal |author=Llinás R, Steinberg IZ, Walton K |title=Relationship between presynaptic calcium current and postsynaptic potential in squid giant synapse |journal=Biophysical Journal |volume=33 |issue=3 |pages=323–351 |year=1981 |pmid=6261850 |doi= |url=http://www.biophysj.org/cgi/pmidlookup?view=long&pmid=6261850 |
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| − | }} |
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| − | </ref> Calcium ions then trigger a biochemical cascade which results in vesicles fusing with the presynaptic membrane and releasing their contents to the synaptic cleft within 180[[microsecond|µsec]] of calcium entry.<ref name="Llinás81"/> Vesicle fusion is driven by the action of a set of proteins in the presynaptic terminal known as [[SNARE (protein)|SNAREs]]. |
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| + | [[Phosphatidylinositol#Phosphoinositides|Phosphoinositides]] ([[Phosphatidylinositol 4-phosphate|PIP]], PIP2, and [[Phosphatidylinositol (3,4,5)-trisphosphate|PIP3]]) are molecules that have been shown to affect neuronal polarity.<ref>{{cite journal |last1=Arimura |first1=Nariko |last2=Kaibuchi |first2=Kozo |date=December 22, 2005 |title=Key regulators in neuronal polarity |journal=[[Neuron (journal)|Neuron]] |volume=48 |issue=6 |pages=881–884 |location=Cambridge, MA |publisher=Cell Press |pmid=16364893 |doi=10.1016/j.neuron.2005.11.007 |accessdate=2013-10-01 |url=http://www.ncbi.nlm.nih.gov/pubmed/16364893}}</ref> They are synthesized by combinational [[phosphorylation]] of [[phosphatidylinositol]] (PI), a [[phospholipid]] cell membrane component. PI is derived from ''myo''-[[inositol]], which is obtained via three pathways: uptake from the extracellular environment, synthesis from [[glucose]], and the recycling of phosphoinositides. Both the synthesis of ''myo''-inositol from glucose and the recycling of phosphoinositides require ''myo''-inositol monophosphatase – IMPase – an enzyme that produces inositol by [[dephosphorylation|dephosphorylating]] [[inositol phosphate]].<ref name="SynapticPolarity">{{cite journal |last1=Kimata |first1=Tsubasa |last2=Tanizawa |first2=Yoshinori |last3=Can |first3=Yoko |last4=Ikeda |first4=Shingo |last5=Kuhara |first5=Atsushi |last6=Mori |first6=Ikue |date=June 1, 2012 |title=Synaptic Polarity Depends on Phosphatidylinositol Signaling Regulated by myo-Inositol Monophosphatase in Caenorhabditis elegans |journal=[[Genetics (journal)|Genetics]] |volume=191 |issue=2 |pages=509–521 |location=Bethesda, MD |publisher=[[Genetics Society of America]] |pmid=22446320 |doi=10.1534/genetics.111.137844 |accessdate=2013-10-01 |url=http://www.ncbi.nlm.nih.gov/pubmed/22446320 |display-authors=3}}</ref> IMPase has been studied ''in vivo'' at some length due to its relevance in the study of [[bipolar disorder]] resulting from its sensitivity to [[Lithium pharmacology|lithium]].<ref>{{cite journal |last=Cade |first=John F. J. |authorlink=John Cade |date=September 3, 1949 |title=Lithium salts in the treatment of psychotic excitement |journal=[[The Medical Journal of Australia]] |volume=2 |issue=10 |pages=349–352 |location=Sydney |publisher=Australasian Medical Publishing Company |pmc=2560740 |accessdate=2013-10-01 |url=http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2560740/}}</ref> In 2006, a gene (''ttx-7'') was identified in ''[[Caenorhabditis elegans]]'' that encodes IMPase. Organisms with mutant ''ttx-7'' genes demonstrated behavioral and localization defects, which were rescued by expression of IMPase and application of inositol. Wild type organisms treated with lithium displayed similar defects to those exhibited by the ''ttx-7'' mutants. This led to the conclusion that IMPase is required for the correct localization of synaptic protein components.<ref>{{cite journal |last1=Tanizawa |first1=Yoshinori |last2=Kuhara |first2=Atsushi |last3=Inada |first3=Hitoshi |last4=Kodama |first4=Eiji |last5=Mizuno |first5=Takafumi |last6=Mori |first6=Ikue |date=December 1, 2006 |title=Inositol monophosphatase regulates localization of synaptic components and behavior in the mature nervous system of C. elegans |journal=[[Genes & Development]] |volume=20 |issue=23 |pages=3296–3310 |location=Cold Spring Harbor, NY |publisher=[[Cold Spring Harbor Laboratory Press]] |pmid=17158747 |pmc=1686606 |doi=10.1101/gad.1497806 |accessdate=2013-10-01 |url=http://www.ncbi.nlm.nih.gov/pubmed/17158747 |display-authors=3}}</ref> |
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| − | The membrane added by this fusion is later retrieved by [[endocytosis]] and [[Endocytic cycle|recycled]] for the formation of fresh neurotransmitter-filled vesicles. |
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| + | The ''egl-8'' gene encodes a homolog of [[phospholipase C]]β (PLCβ), an enzyme that cleaves PIP2. When ''ttx-7'' mutants also had a mutant ''egl-8'' gene, the defects caused by the faulty ''ttx-7'' gene were largely reversed; this suggests that an accumulation of PIP2 corrected the adverse effects of the mutant ''ttx-7'' gene. Furthermore, a mutation in the ''unc-26'' gene (encoding a protein that dephosphorylates PIP2) suppressed the synaptic defects in the ''ttx-7'' mutants. The ''egl-8'' mutants were resistant to lithium treatment. This is genetic evidence that disruption of IMPase alters the levels of PIP2 in neurons; these results suggest that PIP2 signaling establishes polarized localization of synaptic components in living neurons.<ref name="SynapticPolarity" /> |
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| − | ===Receptor binding=== |
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| − | Receptors on the opposite side of the synaptic gap bind neurotransmitter molecules and respond by opening nearby ion channels in the post-synaptic cell membrane, causing ions to rush in or out and changing the local [[transmembrane potential]] of the cell. The resulting change in voltage is called a [[postsynaptic potential]]. In general, the result is ''excitatory'', in the case of [[Depolarization|depolarizing]] currents, or ''inhibitory'' in the case of [[Hyperpolarization|hyperpolarizing]] currents. Whether a synapse is excitatory or inhibitory depends on what type(s) of ion channel conduct the post-synaptic current display(s), which in turn is a function of the type of receptors and neurotransmitter employed at the synapse. |
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| − | |||
| − | ===Termination=== |
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| − | The signal is terminated by either breakdown of neurotransmitters, or reuptake, the latter is mainly in the presynaptic neuron to avail recycling of the transmitter. |
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| − | |||
| − | ====Reuptake==== |
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| − | Following fusion of the synaptic vesicles and release of transmitter molecules into the synaptic cleft, small neurotransmitters, such as [[glycine]], are rapidly cleared from the space for recycling by specialized membrane proteins in the presynaptic or postsynaptic membrane. |
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| − | |||
| − | ====Breakdown==== |
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| − | Some neurotransmitters, e.g. [[acetylcholine]] and large ones such as [[peptides]], are broken down without any direct reuptake. The [[choline]] part of acetylcholine, however, is to a large degree taken up by the presynaptic neuron for recycling. Peptides, on the other hand, must be resynthesized from the neuron [[cell soma|soma]]. |
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| − | |||
| − | == Modulation of synaptic transmission == |
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| − | Synaptic transmission can be modulated by e.g. desensitization, homotropic and heterotropic modulation: |
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| − | |||
| − | ===Desensitization=== |
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| − | {{Main|Desensitization}} |
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| − | Desensitization of the post-synaptic receptors is a decrease in response to the same neurotransmitter stimulus. It means that the strength of a synapse may in effect diminish as a train of action potentials arrive in rapid succession--a phenomenon that gives rise to the so-called frequency dependence of synapses. The nervous system exploits this property for computational purposes, and can tune its synapses through such means as [[phosphorylation]] of the proteins involved. |
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| − | |||
| − | ===Homotropic modulation=== <!--Homotropic modulation redirects here--> |
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| − | Homotropic modulation is a modulation of the presynaptic neuron by its own neurotransmitters, i.e. a form of [[autocrine signaling]]. The modulation can include size, number and replenishment rate of vesicles. It is often inhibitory, with the effect of ''presynaptic inhibition'', making the neurotransmitter self-regulating. |
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| − | |||
| − | One example are neurons of the [[sympathetic nervous system]] (SNS), which release [[noradrenaline]], which, besides from affecting postsynaptic receptors, also affect [[α2-adrenergic receptors]], inhibiting further release of noradrenaline. <ref name=Rang> Pharmacology, (Rang, Dale, Ritter & Moore, ISBN 0443071454, 5:th ed., Churchill Livingstone 2003) Page 129 </ref> This effect is utilized with [[clonidine]] to perform inhibitory effects on the SNS. |
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| − | |||
| − | ===Heterotropic modulation=== <!--Heterotropic modulation redirects here--> |
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| − | Heterotropic modulation is a modulation of presynaptic terminals of nearby neurons. Again, the modulation can include size, number and replenishment rate of vesicles. |
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| − | |||
| − | One example are again neurons of the [[sympathetic nervous system]], which release [[noradrenaline]], which, in addition, generate inhibitory effect on presynaptic terminals of neurons of the [[parasympathetic nervous system]].<ref name=Rang/> |
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| − | |||
| − | ===Pharmacological intervention=== |
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| − | For example, a class of drugs known as selective serotonin [[reuptake]] inhibitors or [[Selective serotonin reuptake inhibitor|SSRI]]s affect certain synapses by inhibiting the reuptake of the neurotransmitter [[serotonin]]. In contrast, one important excitatory neurotransmitter, [[acetylcholine]], is first broken down into [[acetate]] and [[choline]] by the enzyme [[acetylcholinesterase]] prior to removal from the synapse. |
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| − | |||
| − | == Integration of synaptic inputs ==<!-- This section is linked from [[Summation]] --> |
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| − | In general, if an excitatory synapse is strong, an [[action potential]] in the presynaptic neuron will trigger another in the post-synaptic cell, whereas, at a weak synapse, the [[excitatory postsynaptic potential|excitatory post-synaptic potential ("EPSP")]] will not reach the [[action potential|threshold]] for action potential initiation. In the brain, however, each neuron forms synapses with many others, and, likewise, each receives synaptic inputs from many others. When action potentials fire simultaneously in several neurons that weakly synapse on a single cell, they may initiate an impulse in that cell even though the synapses are weak. This process is known as summation.<ref>[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Search&db=books&doptcmdl=GenBookHL&term=synapse+summation+AND+373406%5Buid%5D&rid=mboc4.section.2027#2067 Single Neurons Are Complex Computation Devices] in Chapter 11 of "Molecular Biology of the Cell, 4th Ed." by [[Bruce Alberts]], et al. (2001) Garland Science Textbooks, ISBN 0815332181.</ref> On the other hand, a presynaptic neuron releasing an inhibitory neurotransmitter such as [[GABA]] can cause [[inhibitory postsynaptic potential]] in the post-synaptic neuron, decreasing its excitability and therefore decreasing the neuron's likelihood of firing an action potential. In this way, the output of a neuron may depend on the input of many others, each of which may have a different degree of influence, depending on the strength of its synapse with that neuron. [[John Carew Eccles]] performed some of the important early experiments on synaptic integration, for which he received the [[Nobel Prize for Physiology or Medicine]] in 1963. |
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| − | |||
| − | ==Synaptic strength==<!-- This section is linked from [[Post-synaptic potential]]. See [[WP:MOS#Section management]] --> |
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| − | The strength of a synapse is defined by the change in transmembrane potential resulting from activation of the postsynaptic neurotransmitter receptors. This change in voltage is known as a postsynaptic potential, and is a direct result of ionic [[Current (electricity)|currents]] flowing through the postsynaptic ion channels. Changes in synaptic strength can be short–term and without permanent structural changes in the neurons themselves, lasting seconds to minutes — or long-term ([[long-term potentiation]], or LTP), in which repeated or continuous synaptic activation can result in [[second messenger]] molecules initiating [[protein synthesis]], resulting in alteration of the structure of the synapse itself. Learning and memory are believed to result from long-term changes in synaptic strength, via a mechanism known as [[synaptic plasticity]]. |
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| − | |||
| − | ==Relationship to electrical synapses== |
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| − | An [[electrical synapse]] is a mechanical and electrically conductive link between two abutting [[neuron]]s that is formed at a narrow gap between the pre- and postsynaptic [[cell (biology)|cell]]s known as a [[gap junction]]. At gap junctions, cells approach within about 3.5 [[Nanometre|nm]] of each other, rather than the 20 to 40 nm distance that separates cells at chemical synapses.<ref>Kandel et al., 2000, p. 176</ref><ref>Hormuzdi et al., 2004</ref> As opposed to chemical synapses, the postsynaptic potential in electrical synapses is not caused by the opening of ion channels by chemical transmitters, but by direct electrical coupling between both neurons. Electrical synapses are therefore faster<ref name="KandelPrin"/> and more reliable than chemical synapses. Electrical synapses are found throughout the nervous system, yet are less common than chemical synapses. |
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==See also== |
==See also== |
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| + | *[[Active zone]] |
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| + | *[[Autapse]] |
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*[[Exocytosis]] |
*[[Exocytosis]] |
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*[[Neuromuscular junction]] |
*[[Neuromuscular junction]] |
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*[[Neurotransmitter]] |
*[[Neurotransmitter]] |
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| ⚫ | |||
| + | *[[Neurotransmission]] |
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| + | *[[Postsynaptic density]] |
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*[[Postsynaptic potential]] |
*[[Postsynaptic potential]] |
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:*[[Excitatory postsynaptic potential]] |
:*[[Excitatory postsynaptic potential]] |
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:*[[Inhibitory postsynaptic potential]] |
:*[[Inhibitory postsynaptic potential]] |
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*[[Receptor (biochemistry)|Receptor]] |
*[[Receptor (biochemistry)|Receptor]] |
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| + | *[[Role of the synapse in memory]] |
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| + | *[[Synaptic fatigue]] |
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| + | *[[Synaptic inhibition]] |
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*[[Synaptic pharmacology]] |
*[[Synaptic pharmacology]] |
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| + | *[[Synaptic plasticity]] |
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| + | *[[Synaptic potential]] |
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| + | *[[Synaptic scaling]] |
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| + | *[[Synaptic vesicles]] |
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*[[Synaptogenesis]] |
*[[Synaptogenesis]] |
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| + | *[[Synaptotropic hypothesis]] |
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| + | *[[Types of synapse]] |
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==Notes== |
==Notes== |
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Latest revision as of 12:19, 29 October 2013
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Biological: Behavioural genetics · Evolutionary psychology · Neuroanatomy · Neurochemistry · Neuroendocrinology · Neuroscience · Psychoneuroimmunology · Physiological Psychology · Psychopharmacology (Index, Outline)
In the nervous system, a synapse is a structure that permits a neuron (or nerve cell) to pass an electrical or chemical signal to another cell (neural or otherwise).[1] Santiago Ramón y Cajal proposed that neurons are not continuous throughout the body, yet still communicate with each other, an idea known as the neuron doctrine.[2]
The word "synapse" (from Greek synapsis "conjunction," from synaptein "to clasp," from syn- "together" and haptein "to fasten") was introduced in 1897 by English physiologist Michael Foster at the suggestion of English classical scholar Arthur Woollgar Verrall.[3][4]
Synapses are essential to neuronal function: neurons are cells that are specialized to pass signals to individual target cells, and synapses are the means by which they do so. At a synapse, the plasma membrane of the signal-passing neuron (the presynaptic neuron) comes into close apposition with the membrane of the target (postsynaptic) cell. Both the presynaptic and postsynaptic sites contain extensive arrays of molecular machinery that link the two membranes together and carry out the signaling process. In many synapses, the presynaptic part is located on an axon, but some presynaptic sites are located on a dendrite or soma. Astrocytes also exchange information with the synaptic neurons, responding to synaptic activity and, in turn, regulating neurotransmission.[5]
There are two fundamentally different types of synapses:
- In a chemical synapse, electrical activity in the presynaptic neuron is converted (via the activation of voltage-gated calcium channels) into the release of a chemical called a neurotransmitter that binds to receptors located in the postsynaptic cell, usually embedded in the plasma membrane. The neurotransmitter may initiate an electrical response or a secondary messenger pathway that may either excite or inhibit the postsynaptic neuron. Because of the complexity of receptor signal transduction, chemical synapses can have complex effects on the postsynaptic cell.
- In an electrical synapse, the presynaptic and postsynaptic cell membranes are connected by special channels called gap junctions that are capable of passing electric current, causing voltage changes in the presynaptic cell to induce voltage changes in the postsynaptic cell. The main advantage of an electrical synapse is the rapid transfer of signals from one cell to the next.[6]
Synaptic communication is distinct from ephaptic coupling, in which communication between neurons occurs via indirect electric fields.
Synaptic polarization
The function of neurons depends upon cellular polarization. The distinctive structure of nerve cells allows action potentials to travel directionally (from dendrites to axons), and for these signals to then be received and carried on by post-synaptic neurons or received by effector cells. Nerve cells have long been used as models for cellular polarization, and of particular interest are the mechanisms underlying the polarized localization of synaptic molecules. PIP2 signalling regulated by IMPase plays an integral role in synaptic polarity.
Phosphoinositides (PIP, PIP2, and PIP3) are molecules that have been shown to affect neuronal polarity.[7] They are synthesized by combinational phosphorylation of phosphatidylinositol (PI), a phospholipid cell membrane component. PI is derived from myo-inositol, which is obtained via three pathways: uptake from the extracellular environment, synthesis from glucose, and the recycling of phosphoinositides. Both the synthesis of myo-inositol from glucose and the recycling of phosphoinositides require myo-inositol monophosphatase – IMPase – an enzyme that produces inositol by dephosphorylating inositol phosphate.[8] IMPase has been studied in vivo at some length due to its relevance in the study of bipolar disorder resulting from its sensitivity to lithium.[9] In 2006, a gene (ttx-7) was identified in Caenorhabditis elegans that encodes IMPase. Organisms with mutant ttx-7 genes demonstrated behavioral and localization defects, which were rescued by expression of IMPase and application of inositol. Wild type organisms treated with lithium displayed similar defects to those exhibited by the ttx-7 mutants. This led to the conclusion that IMPase is required for the correct localization of synaptic protein components.[10]
The egl-8 gene encodes a homolog of phospholipase Cβ (PLCβ), an enzyme that cleaves PIP2. When ttx-7 mutants also had a mutant egl-8 gene, the defects caused by the faulty ttx-7 gene were largely reversed; this suggests that an accumulation of PIP2 corrected the adverse effects of the mutant ttx-7 gene. Furthermore, a mutation in the unc-26 gene (encoding a protein that dephosphorylates PIP2) suppressed the synaptic defects in the ttx-7 mutants. The egl-8 mutants were resistant to lithium treatment. This is genetic evidence that disruption of IMPase alters the levels of PIP2 in neurons; these results suggest that PIP2 signaling establishes polarized localization of synaptic components in living neurons.[8]
See also
- Active zone
- Autapse
- Exocytosis
- Neuromuscular junction
- Neurotransmitter
- Neurotransmitter vesicle
- Neurotransmission
- Postsynaptic density
- Postsynaptic potential
- Receptor
- Role of the synapse in memory
- Synaptic fatigue
- Synaptic inhibition
- Synaptic pharmacology
- Synaptic plasticity
- Synaptic potential
- Synaptic scaling
- Synaptic vesicles
- Synaptogenesis
- Synaptotropic hypothesis
- Types of synapse
Notes
- ↑ (2011) Psychology, 2nd, New York: Worth Publishers.
- ↑ (2006) Neuropsychology: Clinical and Experimental Foundations, Boston: Pearson/Allyn & Bacon.
- ↑ synapse. Online Etymology Dictionary. URL accessed on 2013-10-01.
- ↑ Tansey, E.M. (1997). Not committing barbarisms: Sherrington and the synapse, 1897. Brain Research Bulletin 44 (3): 211–212.
- ↑ (August 2009). Tripartite synapses: astrocytes process and control synaptic information. Trends in Neurosciences 32 (8): 421–431.
- ↑ Silverthorn, Dee Unglaub (2007). Human Physiology: An Integrated Approach, Illustration coordinator William C. Ober; illustrations by Claire W. Garrison; clinical consultant Andrew C. Silverthorn; contributions by Bruce R. Johnson, 4th, San Francisco: Pearson/Benjamin Cummings.
- ↑ (December 22, 2005)Key regulators in neuronal polarity. Neuron 48 (6): 881–884.
- ↑ 8.0 8.1 (June 1, 2012)Synaptic Polarity Depends on Phosphatidylinositol Signaling Regulated by myo-Inositol Monophosphatase in Caenorhabditis elegans. Genetics 191 (2): 509–521.
- ↑ Cade, John F. J. (September 3, 1949). Lithium salts in the treatment of psychotic excitement. The Medical Journal of Australia 2 (10): 349–352.
- ↑ (December 1, 2006)Inositol monophosphatase regulates localization of synaptic components and behavior in the mature nervous system of C. elegans. Genes & Development 20 (23): 3296–3310.
References
- Kandel, Eric R.; James H. Schwartz, Thomas M. Jessell (2000). Principles of Neural Science, 4th edition, New York: McGraw-Hill.
- Llinas R. Sugimori M. and Simon S.M. (1982) PNAS 79:2415-2419
- Llinás R, Steinberg IZ, and Walton K (1981). {{{title}}}. Biophysical Journal 33.
- Bear, Mark; Mark F. Bear, Barry W. Connors, Michael A. Paradiso (2001). Neuroscience: Exploring the Brain, Hagerstown, MD: Lippincott Williams & Wilkins.
- Hormuzdi, SG, Filippov MA, Mitropoulou G, Monyer H, Bruzzone R. (Mar 2004). Electrical synapses: a dynamic signaling system that shapes the activity of neuronal networks. Biochim Biophys Acta 1662 (1-2): 113-137.
- Karp, Gerald (2005). Cell and Molecular Biology: concepts and experiments, 4th edition, Hoboken, NJ: John Wiley & Sons, Inc...
- Nicholls, J.G.; Martin A.R., Wallace B.G., Fuchs P.A. (2001). From Neuron to Brain, 4th edition, Sunderland, MA: Sinauer Associates.
External links
- Synapse Review for Kids
- Biologymad.com (2004) Synapses
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