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Chemical synapse

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This article is about chemical synapses of the nervous system. For general information, seesynapse.For other uses, seesynapse (disambiguation).

Chemical synapsesare biological junctions through whichneurons' signals can be sent to each other and to non-neuronal cells such as those inmusclesorglands.Chemical synapses allow neurons to formcircuitswithin thecentral nervous system.They are crucial to thebiological computationsthat underlieperceptionandthought.They allow thenervous systemto connect to and control other systems of the body.

Artistic interpretation of the major elements in chemical synaptic transmission. An electrochemical wave called anaction potentialtravels along theaxonof aneuron.When the action potential reaches the presynaptic terminal, it provokes the release of a synaptic vesicle, secreting its quanta ofneurotransmittermolecules. The neurotransmitter binds to chemical receptor molecules located in the membrane of another neuron, the postsynaptic neuron, on the opposite side of the synaptic cleft.

At a chemical synapse, one neuron releasesneurotransmittermoleculesinto a small space (thesynaptic cleft) that is adjacent to another neuron. The neurotransmitters are contained within small sacs calledsynaptic vesicles,and are released into the synaptic cleft byexocytosis.These molecules then bind toneurotransmitter receptorson the postsynaptic cell. Finally, the neurotransmitters are cleared from the synapse through one of severalpotential mechanismsincluding enzymatic degradation orre-uptakebyspecific transporterseither on the presynaptic cell or on some otherneurogliato terminate the action of the neurotransmitter.

Theadulthumanbrainis estimated to contain from 1014to 5 × 1014(100–500 trillion) synapses.[1]Every cubic millimeter ofcerebral cortexcontains roughly a billion (short scale,i.e. 109) of them.[2]The number of synapses in the humancerebral cortexhas separately been estimated at 0.15 quadrillion (150 trillion)[3]

The word "synapse" was introduced by SirCharles Scott Sherringtonin 1897.[4]Chemical synapses are not the only type of biologicalsynapse:electricalandimmunological synapsesalso exist. Without a qualifier, however, "synapse" commonly refers to chemical synapses.

Structure

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Diagram of a chemical synaptic connection
Further information on formation of synapses:Synaptogenesis

Synapses are functional connections between neurons, or between neurons and other types of cells.[5][6]A typical neuron gives rise to several thousand synapses, although there are some types that make far fewer.[7]Most synapses connectaxonstodendrites,[8][9]but there are also other types of connections, including axon-to-cell-body,[10][11]axon-to-axon,[10][11]anddendrite-to-dendrite.[9]Synapses are generally too small to be recognizable using alight microscopeexcept as points where the membranes of two cells appear to touch, but their cellular elements can be visualized clearly using anelectron microscope.

Chemical synapses pass information directionally from a presynaptic cell to a postsynaptic cell and are therefore asymmetric in structure and function. The presynapticaxon terminal,or synapticbouton, is a specialized area within the axon of the presynaptic cell that containsneurotransmittersenclosed in small membrane-bound spheres calledsynaptic vesicles(as well as a number of other supporting structures and organelles, such asmitochondriaandendoplasmic reticulum). Synaptic vesicles are docked at the presynapticplasma membraneat regions calledactive zones.

Immediately opposite is a region of the postsynaptic cell containing neurotransmitterreceptors;for synapses between two neurons the postsynaptic region may be found on the dendrites or cell body. Immediately behind the postsynaptic membrane is an elaborate complex of interlinked proteins called thepostsynaptic density(PSD).

Proteins in the PSD are involved in anchoring and trafficking neurotransmitter receptors and modulating the activity of these receptors. The receptors and PSDs are often found in specialized protrusions from the main dendritic shaft calleddendritic spines.

Synapses may be described as symmetric or asymmetric. When examined under an electron microscope, asymmetric synapses are characterized by rounded vesicles in the presynaptic cell, and a prominent postsynaptic density. Asymmetric synapses are typically excitatory. Symmetric synapses in contrast have flattened or elongated vesicles, and do not contain a prominent postsynaptic density. Symmetric synapses are typically inhibitory.

Thesynaptic cleft—also calledsynaptic gap—is a gap between the pre- and postsynaptic cells that is about 20 nm (0.02 μ) wide.[12]The small volume of the cleft allows neurotransmitter concentration to be raised and lowered rapidly.[13]

Anautapseis a chemical (or electrical) synapse formed when the axon of one neuron synapses with its own dendrites.

Signaling in chemical synapses

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Overview

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Here is a summary of the sequence of events that take place in synaptic transmission from a presynaptic neuron to a postsynaptic cell. Each step is explained in more detail below. Note that with the exception of the final step, the entire process may run only a few hundred microseconds, in the fastest synapses.[14]

  1. The process begins with a wave of electrochemical excitation called anaction potentialtraveling along the membrane of the presynaptic cell, until it reaches the synapse.
  2. The electricaldepolarizationof the membrane at the synapse causes channels to open that are permeable to calcium ions.
  3. Calcium ions flow through the presynaptic membrane, rapidly increasing the calcium concentration in the interior.
  4. The high calcium concentration activates a set of calcium-sensitive proteins attached tovesiclesthat contain aneurotransmitterchemical.
  5. These proteins change shape, causing the membranes of some "docked" vesicles to fuse with the membrane of the presynaptic cell, thereby opening the vesicles and dumping their neurotransmitter contents into the synaptic cleft, the narrow space between the membranes of the pre- and postsynaptic cells.
  6. The neurotransmitter diffuses within the cleft. Some of it escapes, but some of it binds tochemical receptormolecules located on the membrane of the postsynaptic cell.
  7. The binding of neurotransmitter causes the receptor molecule to beactivatedin some way. Several types of activation are possible, as described in more detail below. In any case, this is the key step by which the synaptic process affects the behavior of the postsynaptic cell.
  8. Due tothermal vibration,the motion of atoms, vibrating about their equilibrium positions in a crystalline solid, neurotransmitter molecules eventually break loose from the receptors and drift away.
  9. The neurotransmitter is either reabsorbed by the presynaptic cell, and then repackaged for future release, or else it is broken down metabolically.

Neurotransmitter release

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Release of neurotransmitter occurs at the end of axonal branches.

The release of a neurotransmitter is triggered by the arrival of a nerve impulse (oraction potential) and occurs through an unusually rapid process of cellular secretion (exocytosis). Within the presynaptic nerve terminal,vesiclescontaining neurotransmitter are localized near the synaptic membrane. The arriving action potential produces an influx ofcalcium ionsthroughvoltage-dependent, calcium-selective ion channelsat the down stroke of the action potential (tail current).[15]Calcium ions then bind tosynaptotagminproteins found within the membranes of the synaptic vesicles, allowing the vesicles to fuse with the presynaptic membrane.[16]The fusion of a vesicle is astochasticprocess, leading to frequent failure of synaptic transmission at the very small synapses that are typical for thecentral nervous system.Large chemical synapses (e.g. theneuromuscular junction), on the other hand, have a synaptic release probability, in effect, of 1.Vesicle fusionis driven by the action of a set of proteins in the presynaptic terminal known asSNAREs.As a whole, the protein complex or structure that mediates the docking and fusion of presynaptic vesicles is called the active zone.[17]The membrane added by the fusion process is later retrieved byendocytosisandrecycledfor the formation of fresh neurotransmitter-filled vesicles.

An exception to the general trend of neurotransmitter release by vesicular fusion is found in the type II receptor cells of mammaliantaste buds.Here the neurotransmitterATPis released directly from the cytoplasm into the synaptic cleft via voltage gated channels.[18]

Receptor binding

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Receptors on the opposite side of the synaptic gap bind neurotransmitter molecules. Receptors can respond in either of two general ways. First, the receptors may directly openligand-gated ion channelsin the postsynaptic cell membrane, causing ions to enter or exit the cell and changing the localtransmembrane potential.[14]The resulting change involtageis called apostsynaptic potential.In general, the result isexcitatoryin the case ofdepolarizingcurrents, andinhibitoryin the case ofhyperpolarizingcurrents. Whether a synapse is excitatory or inhibitory depends on what type(s) of ion channel conduct the postsynaptic current(s), which in turn is a function of the type of receptors and neurotransmitter employed at the synapse. The second way a receptor can affect membrane potential is by modulating the production ofchemical messengersinside the postsynaptic neuron. These second messengers can then amplify the inhibitory or excitatory response to neurotransmitters.[14]

Termination

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After a neurotransmitter molecule binds to a receptor molecule, it must be removed to allow for the postsynaptic membrane to continue to relay subsequentEPSPsand/orIPSPs.This removal can happen through one or more processes:

  • The neurotransmitter may diffuse away due to thermally-induced oscillations of both it and the receptor, making it available to be broken down metabolically outside the neuron or to be reabsorbed.[19]
  • Enzymes within the subsynaptic membrane may inactivate/metabolize the neurotransmitter.
  • Reuptakepumps may actively pump the neurotransmitter back into the presynapticaxon terminalfor reprocessing and re-release following a later action potential.[19]

Synaptic strength

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The strength of a synapse has been defined byBernard Katzas the product of (presynaptic) release probabilitypr,quantal sizeq(the postsynaptic response to the release of a single neurotransmitter vesicle, a 'quantum'), andn,the number of release sites. "Unitary connection" usually refers to an unknown number of individual synapses connecting a presynaptic neuron to a postsynaptic neuron. The amplitude of postsynaptic potentials (PSPs) can be as low as 0.4 mV to as high as 20 mV.[20]The amplitude of a PSP can be modulated byneuromodulatorsor can change as a result of previous activity. Changes in the synaptic strength can be short-term, lasting seconds to minutes, or long-term (long-term potentiation,or LTP), lasting hours. Learning and memory are believed to result from long-term changes in synaptic strength, via a mechanism known assynaptic plasticity.

Receptor desensitization

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Desensitization of the postsynaptic 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 asphosphorylationof the proteins involved.

Synaptic plasticity

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Main article:Synaptic plasticity

Synaptic transmission can be changed by previous activity. These changes are called synaptic plasticity and may result in either a decrease in the efficacy of the synapse, called depression, or an increase in efficacy, called potentiation. These changes can either be long-term or short-term. Forms ofshort-term plasticityincludesynaptic fatigueor depression andsynaptic augmentation.Forms oflong-term plasticityincludelong-term depressionandlong-term potentiation.Synaptic plasticity can be either homosynaptic (occurring at a single synapse) or heterosynaptic (occurring at multiple synapses).

Homosynaptic plasticity

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Main article:Homosynaptic plasticity

Homosynaptic plasticity(or also homotropic modulation) is a change in the synaptic strength that results from the history of activity at a particular synapse. This can result from changes in presynaptic calcium as well as feedback onto presynaptic receptors, i.e. a form ofautocrine signaling.Homosynaptic plasticity can affect the number and replenishment rate of vesicles or it can affect the relationship between calcium and vesicle release. Homosynaptic plasticity can also be postsynaptic in nature. It can result in either an increase or decrease in synaptic strength.

One example is neurons of thesympathetic nervous system(SNS), which releasenoradrenaline,which, besides affecting postsynaptic receptors, also affects presynapticα2-adrenergic receptors,inhibiting further release of noradrenaline.[21]This effect is utilized withclonidineto perform inhibitory effects on the SNS.

Heterosynaptic plasticity

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Main article:Heterosynaptic plasticity

Heterosynaptic plasticity(or also heterotropic modulation) is a change in synaptic strength that results from the activity of other neurons. Again, the plasticity can alter the number of vesicles or their replenishment rate or the relationship between calcium and vesicle release. Additionally, it could directly affect calcium influx. Heterosynaptic plasticity can also be postsynaptic in nature, affecting receptor sensitivity.

One example is again neurons of thesympathetic nervous system,which releasenoradrenaline,which, in addition, generates an inhibitory effect on presynaptic terminals of neurons of theparasympathetic nervous system.[21]

Integration of synaptic inputs

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Main article:Summation (neurophysiology)

In general, if anexcitatory synapseis strong enough, anaction potentialin the presynaptic neuron will trigger an action potential in the postsynaptic cell. In many cases theexcitatory postsynaptic potential(EPSP) will not reach thethresholdfor eliciting an action potential. When action potentials from multiple presynaptic neurons fire simultaneously, or if a single presynaptic neuron fires at a high enough frequency, the EPSPs can overlap and summate. If enough EPSPs overlap, the summated EPSP can reach the threshold for initiating an action potential. This process is known as summation, and can serve as a high pass filter for neurons.[22]

On the other hand, a presynaptic neuron releasing an inhibitory neurotransmitter, such asGABA,can cause aninhibitory postsynaptic potential(IPSP) in the postsynaptic neuron, bringing themembrane potentialfarther away from the threshold, decreasing its excitability and making it more difficult for the neuron to initiate an action potential. If an IPSP overlaps with an EPSP, the IPSP can in many cases prevent the neuron from firing an action potential. In this way, the output of a neuron may depend on the input of many different neurons, each of which may have a different degree of influence, depending on the strength and type of synapse with that neuron.John Carew Ecclesperformed some of the important early experiments on synaptic integration, for which he received theNobel Prize for Physiology or Medicinein 1963.

Volume transmission

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When a neurotransmitter is released at a synapse, it reaches its highest concentration inside the narrow space of the synaptic cleft, but some of it is certain to diffuse away before being reabsorbed or broken down. If it diffuses away, it has the potential to activate receptors that are located either at other synapses or on the membrane away from any synapse. The extrasynaptic activity of a neurotransmitter is known asvolume transmission.[23]It is well established that such effects occur to some degree, but their functional importance has long been a matter of controversy.[24]

Recent work indicates that volume transmission may be the predominant mode of interaction for some special types of neurons. In the mammalian cerebral cortex, a class of neurons calledneurogliaform cellscan inhibit other nearby cortical neurons by releasing the neurotransmitter GABA into the extracellular space.[25]Along the same vein, GABA released from neurogliaform cells into the extracellular space also acts on surroundingastrocytes,assigning a role for volume transmission in the control of ionic and neurotransmitter homeostasis.[26]Approximately 78% of neurogliaform cell boutons do not form classical synapses. This may be the first definitive example of neurons communicating chemically where classical synapses are not present.[25]

Relationship to electrical synapses

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Anelectrical synapseis an electricallyconductivelink between two abuttingneuronsthat is formed at a narrow gap between the pre- and postsynapticcells,known as agap junction.At gap junctions, cells approach within about 3.5nmof each other, rather than the 20 to 40 nm distance that separates cells at chemical synapses.[27][28]As opposed to chemical synapses, the postsynaptic potential in electrical synapses is not caused by the opening of ion channels by chemical transmitters, but rather by direct electrical coupling between both neurons. Electrical synapses are faster than chemical synapses.[13]Electrical synapses are found throughout the nervous system, including in theretina,thereticular nucleus of the thalamus,theneocortex,and in thehippocampus.[29]While chemical synapses are found between both excitatory and inhibitory neurons, electrical synapses are most commonly found between smaller local inhibitory neurons. Electrical synapses can exist between two axons, two dendrites, or between an axon and a dendrite.[30][31]In somefishandamphibians,electrical synapses can be found within the same terminal of a chemical synapse, as inMauthner cells.[32]

Effects of drugs

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Main article:Neuropharmacology

One of the most important features of chemical synapses is that they are the site of action for the majority ofpsychoactive drugs.Synapses are affected by drugs, such as curare, strychnine, cocaine, morphine, alcohol, LSD, and countless others. These drugs have different effects on synaptic function, and often are restricted to synapses that use a specific neurotransmitter. For example,curareis a poison that stopsacetylcholinefrom depolarizing the postsynaptic membrane, causingparalysis.Strychnineblocks the inhibitory effects of the neurotransmitterglycine,which causes the body to pick up and react to weaker and previously ignored stimuli, resulting in uncontrollablemuscle spasms.Morphineacts on synapses that useendorphinneurotransmitters, andalcoholincreases the inhibitory effects of the neurotransmitterGABA.LSDinterferes with synapses that use the neurotransmitterserotonin.Cocaineblocks reuptake ofdopamineand therefore increases its effects.

History and etymology

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During the 1950s,Bernard KatzandPaul Fattobserved spontaneous miniature synaptic currents at the frogneuromuscular junction.[33]Based on these observations, they developed the 'quantal hypothesis' that is the basis for our current understanding of neurotransmitter release asexocytosisand for which Katz received theNobel Prize in Physiology or Medicinein 1970.[34]In the late 1960s,Ricardo Milediand Katz advanced the hypothesis that depolarization-induced influx of calcium ions triggersexocytosis.

Sir Charles Scott Sherringtonincoined the word 'synapse' and the history of the word was given by Sherrington in a letter he wrote to John Fulton:

'I felt the need of some name to call the junction between nerve-cell and nerve-cell... I suggested using "syndesm"... He [Sir Michael Foster] consulted his Trinity friendVerrall,theEuripideanscholar, about it, and Verrall suggested "synapse" (from the Greek "clasp" ).'–Charles Scott Sherrington[4]

See also

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Notes

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  1. ^Drachman D (2005). "Do we have brain to spare?".Neurology.64(12): 2004–5.doi:10.1212/01.WNL.0000166914.38327.BB.PMID15985565.S2CID38482114.
  2. ^Alonso-Nanclares L, Gonzalez-Soriano J, Rodriguez JR, DeFelipe J (September 2008)."Gender differences in human cortical synaptic density".Proc. Natl. Acad. Sci. U.S.A.105(38): 14615–9.Bibcode:2008PNAS..10514615A.doi:10.1073/pnas.0803652105.PMC2567215.PMID18779570.
  3. ^Brain Facts and FiguresWashington University.
  4. ^abCowan, W. Maxwell; Südhof, Thomas C.; Stevens, Charles F. (2003).Synapses.JHU Press. p. 11.ISBN9780801871184.Retrieved9 June2020.
  5. ^ Rapport, Richard L. (2005).Nerve Endings: The Discovery of the Synapse.W. W. Norton & Company. pp. 1–37.ISBN978-0-393-06019-5.
  6. ^ Squire, Larry R.; Floyd Bloom; Nicholas Spitzer (2008).Fundamental Neuroscience.Academic Press. pp. 425–6.ISBN978-0-12-374019-9.
  7. ^ Hyman, Steven E.; Eric Jonathan Nestler (1993).The Molecular Foundations of Psychiatry.American Psychiatric Pub. pp. 425–6.ISBN978-0-88048-353-7.
  8. ^ Smilkstein, Rita (2003).We're Born to Learn: Using the Brain's Natural Learning Process to Create Today's Curriculum.Corwin Press. p. 56.ISBN978-0-7619-4642-7.
  9. ^abLytton, William W. (2002).From Computer to Brain: Foundations of Computational Neuroscience.Springer. p. 28.ISBN978-0-387-95526-1.Axons connecting dendrite to dendrite are dendrodendritic synapses. Axons which connect axon to dendrite are called axodendritic synapses
  10. ^ab Garber, Steven D. (2002).Biology: A Self-Teaching Guide.John Wiley and Sons. p.175.ISBN978-0-471-22330-6.synapses connect axons to cell body.
  11. ^ab Weiss, Mirin; Dr Steven M. Mirin; Dr Roxanne Bartel (1994).Cocaine.American Psychiatric Pub. p. 52.ISBN978-1-58562-138-5.Retrieved2008-12-26.Axons terminating on the postsynaptic cell body are axosomatic synapses. Axons that terminate on axons are axoaxonic synapses
  12. ^Widrow, Bernard; Kim, Youngsik; Park, Dookun; Perin, Jose Krause (2019). "Nature's Learning Rule".Artificial Intelligence in the Age of Neural Networks and Brain Computing.Elsevier. pp. 1–30.doi:10.1016/b978-0-12-815480-9.00001-3.ISBN978-0-12-815480-9.S2CID125516633.
  13. ^abKandel, Schwartz & Jessell 2000,p. 182
  14. ^abcBear, Mark F; Connors, Barry W; Paradiso, Michael A (2007).Neuroscience: exploring the brain.Philadelphia, PA: Lippincott Williams & Wilkins. pp.113–118.
  15. ^ Llinás R, Steinberg IZ, Walton K (1981)."Relationship between presynaptic calcium current and postsynaptic potential in squid giant synapse".Biophysical Journal.33(3): 323–351.Bibcode:1981BpJ....33..323L.doi:10.1016/S0006-3495(81)84899-0.PMC1327434.PMID6261850.
  16. ^Chapman, Edwin R. (2002). "Synaptotagmin: A Ca2+ sensor that triggers exocytosis?".Nature Reviews Molecular Cell Biology.3(7): 498–508.doi:10.1038/nrm855.ISSN1471-0080.PMID12094216.S2CID12384262.
  17. ^Craig C. Garner and Kang Shen. Structure and Function of Vertebrate and Invertebrate Active Zones. Structure and Functional Organization of the Synapse. Ed: Johannes Hell and Michael Ehlers. Springer, 2008.
  18. ^Romanov, Roman A.; Lasher, Robert S.; High, Brigit; Savidge, Logan E.; Lawson, Adam; Rogachevskaja, Olga A.; Zhao, Haitian; Rogachevsky, Vadim V.; Bystrova, Marina F.; Churbanov, Gleb D.; Adameyko, Igor; Harkany, Tibor; Yang, Ruibiao; Kidd, Grahame J.; Marambaud, Philippe; Kinnamon, John C.; Kolesnikov, Stanislav S.; Finger, Thomas E. (2018)."Chemical synapses without synaptic vesicles: Purinergic neurotransmission through a CALHM1 channel-mitochondrial signaling complex".Science Signaling.11(529): eaao1815.doi:10.1126/scisignal.aao1815.ISSN1945-0877.PMC5966022.PMID29739879.
  19. ^abSherwood L., stikawy (2007). Human Physiology 6e: From Cells to Systems
  20. ^Díaz-Ríos M, Miller MW (June 2006)."Target-specific regulation of synaptic efficacy in the feeding central pattern generator of Aplysia: potential substrates for behavioral plasticity?".Biol. Bull.210(3): 215–29.doi:10.2307/4134559.JSTOR4134559.PMID16801496.S2CID34154835.
  21. ^abRang, H.P.; Dale, M.M.; Ritter, J.M. (2003).Pharmacology(5th ed.). Edinburgh: Churchill Livingstone. p. 129.ISBN978-0-443-07145-4.
  22. ^Bruce Alberts; Alexander Johnson; Julian Lewis; Martin Raff; Keith Roberts; Peter Walter, eds. (2002)."Ch. 11. Section: Single Neurons Are Complex Computation Devices".Molecular Biology of the Cell(4th ed.). Garland Science.ISBN978-0-8153-3218-3.
  23. ^Zoli M, Torri C, Ferrari R, et al. (1998). "The emergence of the volume transmission concept".Brain Res. Brain Res. Rev.26(2–3): 136–47.doi:10.1016/S0165-0173(97)00048-9.PMID9651506.S2CID20495134.
  24. ^Fuxe K, Dahlström A, Höistad M, et al. (2007)."From the Golgi-Cajal mapping to the transmitter-based characterization of the neuronal networks leading to two modes of brain communication: wiring and volume transmission"(PDF).Brain Res Rev.55(1): 17–54.doi:10.1016/j.brainresrev.2007.02.009.hdl:10447/9980.PMID17433836.S2CID1323780.
  25. ^abOláh S, Füle M, Komlósi G, et al. (2009)."Regulation of cortical microcircuits by unitary GABA-mediated volume transmission".Nature.461(7268): 1278–81.Bibcode:2009Natur.461.1278O.doi:10.1038/nature08503.PMC2771344.PMID19865171.
  26. ^Rózsa M, Baka J, Bordé S, Rózsa B, Katona G, Tamás G, et al. (2015)."Unitary GABAergic volume transmission from individual interneurons to astrocytes in the cerebral cortex"(PDF).Brain Structure and Function.222(1): 651–659.doi:10.1007/s00429-015-1166-9.PMID26683686.S2CID30728927.
  27. ^Kandel, Schwartz & Jessell 2000,p. 176
  28. ^Hormuzdi et al. 2004
  29. ^Connors BW, Long MA (2004)."Electrical synapses in the mammalian brain".Annu. Rev. Neurosci.27(1): 393–418.doi:10.1146/annurev.neuro.26.041002.131128.PMID15217338.
  30. ^Veruki ML, Hartveit E (December 2002)."Electrical synapses mediate signal transmission in the rod pathway of the mammalian retina".J. Neurosci.22(24): 10558–66.doi:10.1523/JNEUROSCI.22-24-10558.2002.PMC6758447.PMID12486148.
  31. ^Bennett MV, Pappas GD, Aljure E, Nakajima Y (March 1967). "Physiology and ultrastructure of electrotonic junctions. II. Spinal and medullary electromotor nuclei in mormyrid fish".J. Neurophysiol.30(2): 180–208.doi:10.1152/jn.1967.30.2.180.PMID4167209.
  32. ^Pereda AE, Rash JE, Nagy JI, Bennett MV (December 2004). "Dynamics of electrical transmission at club endings on the Mauthner cells".Brain Res. Brain Res. Rev.47(1–3): 227–44.CiteSeerX10.1.1.662.9352.doi:10.1016/j.brainresrev.2004.06.010.PMID15572174.S2CID9527518.
  33. ^Augustine, George J.; Kasai, Haruo (2007-02-01)."Bernard Katz, quantal transmitter release and the foundations of presynaptic physiology".The Journal of Physiology.578(Pt 3): 623–625.doi:10.1113/jphysiol.2006.123224.PMC2151334.PMID17068096.
  34. ^"Nobel prize".British Medical Journal.4(5729): 190. 1970-10-24.doi:10.1136/bmj.4.5729.190.PMC1819734.PMID4320287.

References

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