Editing Synaptic plasticity (section)

==Long-term plasticity==
[[Long-term depression]] (LTD) and [[long-term potentiation]] (LTP) 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"/>
The turning point for the synaptic modification of a synapse has been found to be modifiable itself, depending on the history of the synapse.<ref name="pmid7619513">{{cite journal | vauthors = Bear MF | title = Mechanism for a sliding synaptic modification threshold | journal = Neuron | volume = 15 | issue = 1 | pages = 1–4 | date = July 1995 | pmid = 7619513 | doi = 10.1016/0896-6273(95)90056-x | doi-access = free }}</ref> Recently, a number of attempts have been made to offer a comprehensive model that could account for most forms of synaptic plasticity.<ref name="pmid21348800">{{cite journal | vauthors = Michmizos D, Koutsouraki E, Asprodini E, Baloyannis S | title = Synaptic plasticity: a unifying model to address some persisting questions | journal = The International Journal of Neuroscience | volume = 121 | issue = 6 | pages = 289–304 | date = June 2011 | pmid = 21348800 | doi = 10.3109/00207454.2011.556283 | s2cid = 24610392 }}</ref>

===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"/>
Activity-dependent LTD was investigated in 2011 for the electrical synapses (modification of Gap Junctions efficacy through their activity).<ref name="pmid22021860">{{cite journal | vauthors = Haas JS, Zavala B, Landisman CE | title = Activity-dependent long-term depression of electrical synapses | journal = Science | volume = 334 | issue = 6054 | pages = 389–93 | date = October 2011 | pmid = 22021860 | doi = 10.1126/science.1207502 | bibcode = 2011Sci...334..389H | s2cid = 35398480 | pmc = 10921920 }}</ref> In the brain, cerebellum is one of the structures where LTD is a form of neuroplasticity.<ref>{{cite journal | vauthors = Mitoma H, Kakei S, Yamaguchi K, Manto M | title = Physiology of Cerebellar Reserve: Redundancy and Plasticity of a Modular Machine | journal = Int. J. Mol. Sci. | volume = 22 | pages = 4777 |  date = April 2021 | issue = 9 | doi = 10.3390/ijms22094777 | pmid = 33946358 | pmc = 8124536 | doi-access = free }}</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. 
The long-term stabilization of synaptic changes is determined by a parallel increase of pre- and postsynaptic structures such as [[Bouton (synapse)|axonal bouton]], [[dendritic spine]] and [[postsynaptic density]].<ref name="stabilization_plasticity" />
On the molecular level, an increase of the postsynaptic scaffolding proteins [[PSD-95]] and [[HOMER1|Homer1c]] has been shown to correlate with the stabilization of synaptic enlargement.<ref name="stabilization_plasticity" />

Modification of astrocyte coverage at the synapses in the hippocampus has been found to result from the [[LTP induction|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 | vauthors = Artola A, Singer W | title = Long-term depression of excitatory synaptic transmission and its relationship to long-term potentiation | journal = Trends in Neurosciences | volume = 16 | issue = 11 | pages = 480–7 | date = November 1993 | pmid = 7507622 | doi = 10.1016/0166-2236(93)90081-V | s2cid = 3974242 }}</ref> Experiments performed by stimulating an array of individual dendritic spines, have shown that synaptic cooperativity by as few as two adjacent dendritic spines prevents LTD, allowing only LTP.<ref>{{cite journal|vauthors=Tazerart S, Mitchell DE, Miranda-Rottmann S, Araya R|date=August 2020|title=A spike-timing-dependent plasticity rule for dendritic spines|journal=Nature Communications|volume=11|issue=1|pages=4276|doi=10.1038/s41467-020-17861-7|pmc=7449969|pmid=32848151|bibcode=2020NatCo..11.4276T}}</ref>