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{{for|the general concept of brain plasticity|neuroplasticity}}

In [[neuroscience]], '''synaptic plasticity''' is the ability of [[synapses]] to [[Chemical synapse#Synaptic strength|strengthen or weaken]] over time, in response to increases or decreases in their activity.<ref>{{cite journal |last=Hughes |first=John R. |year=1958
  |title=Post-tetanic Potentiation
  |url=
  |journal=Physiological Reviews
  |volume=38
  |issue=
  1
|pages=91–113 |pmid=13505117 }}</ref> Plastic change also results from the alteration of the number of receptors located on a synapse.<ref name="NewT">{{cite journal |doi=10.1016/j.conb.2010.06.010 |last=Gerrow |first=Kimberly |coauthors=Antoine  |year=2010
  |title=Synaptic stability and plasticity in a floating world
  |url=
  |journal=Current Opinion in Neurobiology
  |volume=20
  |issue=
  5
|pages=631–639 |pmid=20655734 }}</ref> There are several underlying mechanisms that cooperate to achieve synaptic plasticity, including changes in the quantity of [[neurotransmitter]]s released into a synapse and changes in how effectively cells respond to those neurotransmitters.<ref>
{{cite journal
  |last=Gaiarsa
  |first=J.L.
  |coauthors=Caillard O., and Ben-Ari Y.
  |year=2002
  |title=Long-term plasticity at GABAergic and glycinergic synapses: mechanisms and functional significance
  |url=
  |journal=Trends in Neurosciences
  |volume=25
  |issue=11
  |pages=564–570
  |doi=10.1016/S0166-2236(02)02269-5
  |pmid=12392931}}</ref> Synaptic plasticity in both excitatory and inhibitory synapses has been found to be dependent upon postsynaptic [[calcium]] release.<ref name="NewT"/> Since [[memory|memories]] are postulated to be represented by vastly interconnected networks of synapses in the [[brain]], synaptic plasticity is one of the important neurochemical foundations of [[learning]] and [[memory]] (''see [[Hebbian theory]]'').

==Historical discoveries==
In 1973, Terje Lømo and Tim Bliss first described the now widely studied phenomenon of [[long-term potentiation]] (LTP) in a publication in the ''Journal of Physiology''. The experiment described was conducted on the synapse between the perforant path and dentate gyrus in the hippocampi of anaesthetised rabbits. They were able to show a burst of tetanic (100&nbsp;Hz) stimulus on perforant path fibres led to a dramatic and long-lasting augmentation in the post-synaptic response of cells onto which these fibres synapse in the dendate gyrus. In the same year, the pair published very similar data recorded from awake rabbits. This discovery was of particular interest due to the proposed role of the hippocampus in certain forms of memory.

==Biochemical mechanisms==
Two molecular mechanisms for synaptic plasticity (researched by the [[Eric Kandel]] laboratories) involve the [[NMDA]] and [[AMPA]] glutamate receptors.  Opening of NMDA channels (which relates to the level of cellular depolarization) leads to a rise in post-synaptic Ca<sup>2+</sup> concentration and this has been linked to long-term potentiation, LTP (as well as to protein kinase activation); strong depolarization of the post-synaptic cell completely displaces the magnesium ions that block NMDA ion channels and allows calcium ions to enter a cell – probably causing LTP, while weaker depolarization only partially displaces the Mg<sup>2+</sup> ions, resulting in less Ca<sup>2+</sup> entering the post-synaptic neuron and lower intracellular Ca<sup>2+</sup> concentrations (which activate protein phosphatases and induce long-term depression, LTD).<ref>Bear MF, Connors BW, and Paradisio MA. 2007. Neuroscience: Exploring the Brain, 3rd ed. Lippincott, Williams & Wilkins</ref>  

These activated protein kinases serve to phosphorylate post-synaptic excitatory receptors (e.g. [[AMPA receptor]]s), improving cation conduction, and thereby potentiating the synapse. Also, this signals recruitment of additional receptors into the post-synaptic membrane, and stimulates the production of a modified receptor type, thereby facilitating an influx of calcium. This in turn increases post-synaptic excitation by a given pre-synaptic stimulus.  This process can be reversed via the activity of protein phosphatases, which act to dephosphorylate these cation channels.<ref>{{cite journal | doi = 10.1016/S0166-2236(99)01490-3 | last1 = Soderling | first1 = TR | last2 = Derkach | first2 = VA | author-separator =, | author-name-separator= | year = 2000 | title = Postsynaptic protein phosphorylation and LTP | url = | journal = [[Trends in Neurosciences]] | volume = 23 | issue = 2| pages = 75–80 | pmid = 10652548 }}</ref> 

The second mechanism depends on a [[second messenger]] cascade regulating [[Transcription (genetics)|gene transcription]] and changes in the levels of key proteins at synapses such as CaMKII and PKAII. Activation of the second messenger pathway leads to increased levels of CaMKII and PKAII within the dendritic spine. These protein kinases have been linked to growth in dendritic spine volume and LTP processes such as the addition of AMPA receptors to the plasma membrane and phosphorylation of ion channels for enhanced permeability.<ref name="Haining09">
{{cite journal
  |last=Haining
  |first=Z.
  |coauthors=Sia G., Sato T., Gray N., Mao T., Khuchia Z., Huganir R., Svodoba K.
  |year=2009
  |title=Subcellular Dynamics of Type II PKA in Neurons
  |url=
  |journal=Cell Press
  |issn=
  |volume=62
  |issue=
  |pages=363–374
  |pmid=}}</ref> Localization or compartmentalization of activated proteins occurs in the presence of their given stimulus which creates local effects in the dendritic spine. Calcium influx from NMDA receptors is necessary for the activation of CaMKII. This activation is localized to spines with focal stimulation and is inactivated before spreading to adjacent spines or the shaft, indicating an important mechanism of LTP in that particular changes in protein activation can be localized or compartmentalized to enhance the responsivity of single dendritic spines. Individual dendritic spines are capable of forming unique responses to presynaptic cells.<ref name="Seok-Jin09">
{{cite journal
  |doi=10.1038/nature07842
  |last=Seok-Jin
  |first=R.
  |coauthors=Escobedo-Lozoya Y., Szatmari E., Yasuda R.
  |year=2009
  |title=Activation of CaMKII in single dendritic spines during long-term potentiation
  |pmc=2719773
  |url=
  |journal=Nature
  |issn=
  |volume=458
  |issue=19
  |pages=299–306
  |pmid=19295602}}</ref> This second mechanism can be triggered by protein phosphorylation but takes longer and lasts longer, providing the mechanism for long-lasting memory storage.  The duration of the LTP can be regulated by breakdown of these [[second messenger]]s.  [[Phosphodiesterase]], for example, breaks down the secondary messenger [[Cyclic adenosine monophosphate|cAMP]], which has been implicated in increased AMPA receptor synthesis in the post-synaptic neuron {{Citation needed|date=December 2011}}.

Long-lasting changes in the efficacy of synaptic connections ([[long-term potentiation]], or LTP) between two neurons can involve the making and breaking of synaptic contacts. Genes such as activin ß-A, which encodes a subunit of activin A, are up-regulated during early stage LTP. The activin molecule modulates the actin dynamics in dendritic spines through the MAP kinase pathway. By changing the F-actin cytoskeletal structure of dendritic spines, spines are lengthened and the chance that they make synaptic contacts with the axonal terminals of the presynaptic cell is increased. The end result is long term maintenance of LTP.<ref name="Synapse">
{{cite journal
  |doi=10.1242/jcs.012450
  |last=Shoji-Kasai
  |first=Yoko
  |coauthors= Hiroshi Ageta, Yoshihisa Hasegawa, Kunihiro Tsuchida, Hiromu Sugino, Kaoru Inokuchi
  |year=2007
  |title=Activin increases the number of synaptic contacts and the length of dendritic spine necks by modulating spinal actin dynamics
  |url=http://assets0.pubget.com/pdf/17940062.pdf
  |journal=Journal of Cell Science
  |issn=
  |volume=120
  |issue=
  Pt 21
|pages=3830–3837
  |pmid=17940062}}</ref>

The number of ion channels on the post-synaptic membrane affects the strength of the synapse.<ref>
{{cite journal
  |last=Debanne
  |first=D.
  |coauthors=Daoudal G., Sourdet V., and Russier M.
  |year=2003
  |title=Brain plasticity and ion channels
  |url=
  |journal=Journal of Physiology, Paris
  |volume=97
  |issue=4-6
  |pages=403–414
  |doi=10.1016/j.jphysparis.2004.01.004
  |pmid=15242652}}</ref> Research suggests that the density of receptors on post-synaptic membranes changes, affecting the neuron’s excitability in response to stimuli. In a dynamic process that is maintained in equilibrium, [[NMDA receptor|N-methyl D-aspartate receptor (NMDA receptor)]] and AMPA receptors are added to the membrane by [[exocytosis]] and removed by [[endocytosis]].<ref name="Shi99">
{{cite journal
  |last=Shi
  |first=S.H.
  |coauthors=Hayashi Y., Petralia R.S., Zaman S.H., Wenthold R., Svoboda K., Malinow R.
  |year=1999
  |title=Rapid spine delivery and redistribution of AMPA receptors after synaptic NMDA receptor activation
  |url=
  |journal=Science
  |issn=0193-4511
  |volume=284
  |issue=5421
  |pages=1811–1816
  |pmid=10364548
|doi=10.1126/science.284.5421.1811}}</ref><ref name="Song02">
{{cite journal
  |last=Song
  |first=I.
  |coauthors=Huganir R.L.
  |year=2002
  |title=Regulation of AMPA receptors during synaptic plasticity
  |url=
  |journal=Trends in Neurosciences
  |volume=25
  |issue=11
  |pages=578–589
  |doi=10.1016/S0166-2236(02)02270-1
|pmid=12392933}}</ref><ref name="PO05">
{{cite journal
  |last=Pérez-Otaño
  |first=I.
  |coauthors=Ehlers M.D.
  |year=2005
  |title=Homeostatic plasticity and NMDA receptor trafficking
  |url=http://www.psychiatry.wustl.edu/zorumski/journal%20club/Perez-Otano%20and%20Ehlers%209_23.pdf
  |format=[[PDF]]
  |journal=Trends in Neurosciences
  |volume=28
  |issue=5
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  |accessdate=2007-06-08
  |doi=10.1016/j.tins.2005.03.004
  |pmid=15866197}} {{Dead link|date=November 2010|bot=H3llBot}}</ref> These processes, and by extension the number of receptors on the membrane, can be altered by synaptic activity.<ref name="Shi99" /><ref name="PO05" /> Experiments have shown that AMPA receptors are delivered to the synapse through vesicular membrane fusion with the postsynaptic membrane via the protein kinase CaMKII, which is activated by the influx of calcium through NMDA receptors. CaMKII also improves AMPA ionic conductance through phosphorylation.<ref name="renamed_from_450_on_20101201190949">{{cite book
  | last = Bear
  | first = M.F.
  | authorlink = Mark F. Bear
  | title = Neuroscience: Exploring the Brain
  | publisher = [[Lippincott Williams & Wilkins]]
  | series = Third Edition
  | year =2007
  | pages =779
  | isbn = 978-0-7817-6003-4}}</ref>
When there is high-frequency NMDA receptor activation, there is an increase in the expression of a protein PSD-95 that increases synaptic capacity for AMPA receptors. This is what leads to a long-term increase in AMPA receptors and thus synaptic strength and plasticity.

If the strength of a synapse is only reinforced by stimulation or weakened by its lack, a positive feedback loop will develop, causing some cells never to fire and some to fire too much.  But two regulatory forms of plasticity, called scaling and [[metaplasticity]], also exist to provide negative feedback.<ref name="PO05" />  Synaptic scaling is a primary mechanism by which a neuron is able to stabilize firing rates up or down.<ref>
{{cite journal
  |last=Desai
  |first=Niraj S.
  |coauthors=Robert H. Cudmore, Sacha B. Nelson & Gina G. Turrigiano
  |year=2002
  |title=Critical periods for experience-dependent synaptic scaling in visual cortex
  |url=http://www.nature.com/neuro/journal/v5/n8/abs/nn878.html
  |journal=Nature Neuroscience
  |pmid=12080341
  |volume=5
  |issue=
  8
|pages=783–789
  |doi=10.1038/nn878}}</ref>
  
Synaptic scaling serves to maintain the strengths of synapses relative to each other, lowering amplitudes of small excitatory [[postsynaptic potential]]s in response to continual excitation and raising them after prolonged blockage or inhibition.<ref name="PO05" /> This effect occurs gradually over hours or days, by changing the numbers of [[NMDA receptor]]s at the synapse (Pérez-Otaño and Ehlers, 2005).  [[Metaplasticity]] varies the threshold level at which plasticity occurs, allowing integrated responses to synaptic activity spaced over time and preventing saturated states of LTP and LTD.  Since LTP and LTD ([[long-term depression]]) rely on the influx of [[Calcium in biology|Ca<sup>2+</sup>]] through NMDA channels, metaplasticity may be due to changes in NMDA receptors, altered calcium buffering, altered states of kinases or phosphatases and a priming of protein synthesis machinery.<ref name="Abraham97">{{cite journal
  |doi=10.1016/S0301-0082(97)00018-X
  |last=Abraham
  |first=Wickliffe
  |coauthors=Warren P. Tate
  |year=1997
  |title=Metaplasticity: A new vista across the field of synaptic plasticity
  |journal=Progress in Neurobiology
  |volume=52
  |issue=4
  |pages=303–323
  |pmid=9247968}}</ref> Synaptic scaling is a primary mechanism by which a neuron to be selective to its varying inputs.<ref name="Abbot2000">
{{cite journal
  |last=Abbott
  |first=L.
  |coauthors=Sacha B. Nelson
  |year=2000
  |title=Synaptic plasticity: taming the beast
  |url=http://www.nature.com/neuro/journal/v3/n11s/full/nn1100_1178.html
  |journal=Nature Neuroscience
  |pmid=11127835
  |volume=3
  |issue=
  |pages=1178–1183
  |doi=10.1038/81453}}</ref>
The neuronal circuitry affected by LTP/LTD and modified by scaling and metaplasticity leads to reverberatory neural circuit development and regulation in a Hebbian manner which is manifested as memory, whereas the changes in neural circuitry, which begin at the level of the synapse, are an integral part in the ability of an organism to learn.<ref>
{{cite journal
  |last=Cooper
  |first=Stephen J.
  |coauthors=
  |year=2005
  |title=Donald O. Hebb's synapse and learning rule: a history and commentary 
  |url=http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T0J-4DTK9XF-1&_user=130907&_coverDate=01%2F01%2F2005&_rdoc=1&_fmt=high&_orig=search&_origin=search&_sort=d&_docanchor=&view=c&_searchStrId=1560388383&_rerunOrigin=scholar.google&_acct=C000004198&_version=1&_urlVersion=0&_userid=130907&md5=8ac0971cf8fe2a34de02d0886ab00820&searchtype=a#SECX13
  |journal=Neuroscience and Biobehavioral Reviews
  |pmid=15642626
  |volume=28
  |issue=8
  |pages=851–874
  |doi=10.1016/j.neubiorev.2004.09.009}}</ref>  

There is also a specificity element of biochemical interactions to create synaptic plasticity, namely the importance of location. Processes occur at microdomains – such as exocytosis of AMPA receptors is spatially regulated by the t-SNARE Stx4.<ref>{{Cite journal
  | last = Kennedy
  | first = Matthew J.
  | coauthors = Ian G. Davison, Camenzind G. Robinson, and Michael D. Ehlers
  | title = Syntaxin-4 Defines a Domain for Activity-Dependent Exocytosis in Dendritic Spines
  | journal = Cell
  | volume = 141
  | issue = 3
  | pages = 1–12
  | publisher = Elsevier Inc.
  | year = 2010
  | doi = 10.1016/j.cell.2010.02.042
  | pmid=20434989}}</ref>
Specificity is also an important aspect of CAMKII signaling involving nanodomain calcium.<ref>
{{Cite journal
  | last = Lee
  | first = Seok-Jin R.
  | coauthors = Yasmin Escobedo-Lozoya, Erzsebet M. Szatmari, and Ryohei Yasuda
  | title = Activation of CaMKII in single dendritic spines during long-term potentiation
  | journal = Nature
  | volume = 458
  | issue = 7236
  | pages = 299–304
  | publisher = Macmillan Publishers Limited
  | year = 2009
  | pmid = 19295602
  | pmc = 2719773
  | doi = 10.1038/nature07842}}</ref>
The spatial gradient of PKA between dendritic spines and shafts is also important for the strength and regulation of synaptic plasticity.<ref name="Haining09"/>  It is important to remember that the biochemical mechanisms altering synaptic plasticity occur at the level of individual synapses of a neuron.  Since the biochemical mechanisms are confined to these "microdomains," the resulting synaptic plasticity affects only the specific synapse at which it took place.

==Theoretical mechanisms==
A bidirectional model, describing both LTP and LTD, of synaptic plasticity has proved necessary for a number of different learning mechanisms in [[computational neuroscience]], [[neural networks]], and [[biophysics]]. Three major hypotheses for the molecular nature of this plasticity have been well-studied, and none are required to be the exclusive mechanism:
# Change in the probability of glutamate release.
# Insertion or removal of post-synaptic AMPA receptors.
# [[Phosphorylation]] and de-phosphorylation inducing a change in AMPA receptor conductance.

Of these, the first two hypotheses have been recently mathematically examined to have identical calcium-dependent dynamics which provides strong theoretical evidence for a calcium-based model of plasticity, which in a linear model where the total number of receptors are conserved looks like

:<math>\frac{d W_i(t)}{d t}=\frac{1}{\tau([Ca^{2+}]_i)}\left(\Omega([Ca^{2+}]_i)-W_i\right),</math>

where <math>W_i</math> is the [[synaptic weight]] of the <math>i</math>th input axon, <math>\tau</math> is a time constant dependent on the insertion and removal rates of neurotransmitter receptors, which is dependent on <math>[Ca^{2+}]</math>, the concentration of calcium. <math>\Omega=\beta A_m^{\rm fp}</math> is also a function of the concentration of calcium that depends linearly on the number of receptors on the membrane of the neuron at some fixed point. Both <math>\Omega</math> and <math>\tau</math> are found experimentally and agree on results from both hypotheses. The model makes important simplifications that make it unsuited for actual experimental predictions, but provides a significant basis for the hypothesis of a calcium-based synaptic plasticity dependence.<ref>{{cite journal |last=Shouval |first=Harel Z. |coauthors=Gastone C. Castellani, Brian S. Blais, Luk C. Yeung, [[Leon Cooper|Leon N. Cooper]] |year=2002 |month= |title=Converging evidence for a simplified biophysical model of synaptic plasticity |journal=Biological Cybernetics |volume=87 |issue= 5-6|pages=383–391 |id= |url=http://physics.brown.edu/physics/researchpages/Ibns/Lab%20Publications%20(PDF)/converging.pdf |accessdate= 2007-11-12 |quote=|doi=10.1007/s00422-002-0362-x |pmid=12461628 }}</ref>

==Short-term plasticity==
Short-term synaptic plasticity acts on a timescale of tens of milliseconds to a few minutes unlike long-term plasticity, which lasts from minutes to hours. Short term plasticity can either strengthen or weaken a synapse.

===Synaptic enhancement===
Short-term synaptic enhancement results from an increased probability of synaptic terminals releasing transmitters in response to pre-synaptic action potentials. Synapses will strengthen for a short time because of either an increase in size of the readily releasable pool of packaged transmitter or an increase in the amount of packaged transmitter released in response to each action potential.<ref>{{cite doi|10.1016/S0896-6273(00)80685-6}}</ref> Depending on the time scales over which it acts synaptic enhancement is classified as [[neural facilitation]], [[synaptic augmentation]] or [[post-tetanic potentiation]].

===Synaptic depression===
[[Synaptic fatigue]] or depression is usually attributed to the depletion of the readily releasable vesicles. Depression can also arise from post-synaptic processes and from feedback activation of presynaptic receptors.<ref>{{cite journal |last=Zucker |first=Robert S. |year=2002 |last2=Regehr |month=Mar |first2=WG |title=Short-term Synaptic Plasticity |journal=Annual Review of Physiology |volume=64 |issue= |pages=355–405 |id= |url=http://www.annualreviews.org/doi/abs/10.1146/annurev.physiol.64.092501.114547 |accessdate= 2010-11-27 | doi=10.1146/annurev.physiol.64.092501.114547
 | pmid=11826273 }}</ref>
[[Heterosynaptic]] depression is thought to be linked to the release of [[adenosine triphosphate]] (ATP) from [[astrocyte]]s.<ref name="Glia">{{cite journal 
  |last=Achour
  |first=S. Ben 
  |coauthor=O. Pascaul
  |date=Mar 2010
  |title=Glia: The many ways to modulate synaptic plasticity
  |journal=Neurochemistry International
  |volume=57
  |issue=  4
  |pmid=20193723|pages=440–445 
  |id= 
  |url=
  |accessdate= 2010-11-28
  |doi=10.1016/j.neuint.2010.02.013 }}</ref>

==Long-term plasticity==
[[Long-term depression]] and [[long-term potentiation]] are two forms of long-term plasticity, lasting minutes or more, that occur at excitatory synapses.<ref name="NewT"/> NMDA-dependent LTD and LTP have been extensively researched, and are found to require the binding of [[glutamate]], and [[glycine]] or [[D-serine]] for activation of NMDA receptors.<ref name="Glia"/>

===Long-term depression===
Brief activation of an excitatory pathway can produce what is known as long-term depression (LTD) of synaptic transmission in many areas of the brain. LTD is induced by a minimum level of postsynaptic depolarization and simultaneous increase in the intracellular calcium concentration at the postsynaptic neuron. LTD can be initiated at inactive synapses if the calcium concentration is raised to the minimum required level by heterosynaptic activation, or if the extracellular concentration is raised. These alternative conditions capable of causing LTD differ from the Hebb rule, and instead depend on synaptic activity modifications. [[D-serine]] release by [[astrocyte]]s has been found to lead to a significant reduction of LTD in the hippocampus.<ref name="Glia"/>
A LTD was evidenced in 2011 for the electrical synapses (modification of Gap Junctions efficacy through their activity).<ref>J. S. Haas, B. Zavala, C. E. Landisman, Activity-dependent long-term depression of electrical synapses" ''Science'' 334, 389–393 (2011). [Abstract] [Full Text]</ref>

===Long-term potentiation===
Long-term potentiation, commonly referred to as LTP, is an increase in synaptic response following potentiating pulses of electrical stimuli that sustains at a level above the baseline response for hours or longer. LTP involves interactions between postsynaptic neurons and the specific presynaptic inputs that form a synaptic association, and is specific to the stimulated pathway of synaptic transmission. Modification of astrocyte coverage at the synapses in the hippocampus has been found to result from the induction of LTP, which has been found to be linked to the release of [[D-serine]], [[nitric oxide]], and the [[chemokine]], [[s100B]] by [[astrocyte]]s.<ref name="Glia"/>
LTP is also a model for studying the synaptic basis of Hebbian plasticity. Induction conditions resemble those described for the initiation of long-term depression (LTD), but a stronger depolarization and a greater increase of calcium are necessary to achieve LTP.<ref>
{{cite journal 
  |last=Artola 
  |first=Alain 
  |coauthor=Wolf Singer
  |year=1993 
  |month=
  |title=Long-term depression of excitatory synaptic transmission and its relationship to long-term potentiation 
  |journal=Trends in Neuroscience 
  |volume=16 
  |issue=11 
  |pages=480–487 
  |id= 
  |url=http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T0V-485RJH4-C6&_user=10&_coverDate=11%2F30%2F1993&_rdoc=1&_fmt=high&_orig=search&_origin=search&_sort=d&_docanchor=&view=c&_searchStrId=1559086874&_rerunOrigin=scholar.google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=7348dc4a1f08c5337549f42612209812&searchtype=a
  |accessdate= 2010-11-28
  |doi=10.1016/0166-2236(93)90081-V  }}</ref>

==Synaptic strength==
The modification of [[synaptic strength]] is referred to as functional plasticity. Changes in synaptic strength involve distinct mechanisms of particular types of [[glial cell]]s, the most researched type being [[astrocyte]]s.<ref name="Glia"/>

==See also==
* [[BCM theory]]
* [[Excitatory postsynaptic potential]]
* [[Homosynaptic Plasticity]]
* [[Heterosynaptic Plasticity]]
* [[Homeostatic plasticity]]
* [[Inhibitory postsynaptic potential]]
* [[Long-term potentiation]] (LTP)
* [[Long-term depression]] (LTD)
* [[Activity-dependent plasticity]]
* [[Spike-timing-dependent plasticity]] (STDP)
* [[Synaptic augmentation]] (Short-term plasticity)
* [[Neural facilitation]] (Short-term plasticity)
* [[Neuroplasticity]]
* [[Postsynaptic potential]]
* [[Non-synaptic plasticity]]

==References==
{{reflist|colwidth=35em}}

==Bibliography==
* {{cite journal|last=Thornton|first=James K.|coauthors=|year=2003|title=New LSD Research: Gene Expression within the Mammalian Brain |url=http://www.maps.org/news-letters/v13n1/13124tho.html|journal=MAPS|issn=|volume=13|issue=1|pages=|accessdate=2007-06-08}}
* [[Georges Chapouthier|Chapouthier, G.]] (2004). From the search for a molecular code of memory to the role of neurotransmitters: a historical perspective, Neural Plasticity, 11(3-4), 151-158
* Hawkins, R.D., Kandel, E.R., & Bailey, C.H. (June 2006). Molecular Mechanisms of Memory Storage in Aplysia. Biological Bulletin, 210, 174-191.
* LeDoux, Joseph. Synaptic Self: How Our Brains Become Who We Are. New York: Penguin Books, 2002. 1-324. Print.

==External links==
* [http://icwww.epfl.ch/~gerstner//SPNM/node71.html Overview]
* [http://cnr.iop.kcl.ac.uk/default.aspx?pageid=169 Finnerty lab, MRC Centre for Neurodegeneration Research, London]
*[http://www.bris.ac.uk/synaptic/public/plasticity.htm Brain Basics Synaptic Plasticity Synaptic transmission is plastic]
* [http://nba.uth.tmc.edu/neuroscience/s1/chapter07.html Synaptic Plasticity], ''Neuroscience Online'' (electronic neuroscience textbook by UT Houston Medical School)

=== Videos, podcasts ===
* [http://videocast.nih.gov/Summary.asp?file=13746 Synaptic plasticity: Multiple mechanisms and functions] - a lecture by Robert Malenka, M.D., Ph.D., [[Stanford University]]. Video podcast, runtime: 01:05:17.

{{Nervous system physiology}}

{{DEFAULTSORT:Synaptic Plasticity}}
[[Category:Memory processes]]
[[Category:Neuroscience]]
[[Category:Neurology]]
[[Category:Neurophysiology]]
[[Category:Neural networks]]

[[es:Neuroplasticidad]]