Synaptic plasticity

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Synaptic plasticity rule for gradient estimation by dynamic perturbation of conductances Synaptic Plasticity Rule.png
Synaptic plasticity rule for gradient estimation by dynamic perturbation of conductances

In neuroscience, synaptic plasticity is the ability of synapses to strengthen or weaken over time, in response to increases or decreases in their activity. [1] Since memories are postulated to be represented by vastly interconnected neural circuits in the brain, synaptic plasticity is one of the important neurochemical foundations of learning and memory (see Hebbian theory ).

Contents

Plastic change often results from the alteration of the number of neurotransmitter receptors located on a synapse. [2] There are several underlying mechanisms that cooperate to achieve synaptic plasticity, including changes in the quantity of neurotransmitters released into a synapse and changes in how effectively cells respond to those neurotransmitters. [3] Synaptic plasticity in both excitatory and inhibitory synapses has been found to be dependent upon postsynaptic calcium release. [2]

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 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 dentate 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 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 Ca2+ 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 Mg2+ ions, resulting in less Ca2+ entering the post-synaptic neuron and lower intracellular Ca2+ concentrations (which activate protein phosphatases and induce long-term depression, LTD). [4]

These activated protein kinases serve to phosphorylate post-synaptic excitatory receptors (e.g. AMPA receptors), improving cation conduction, and thereby potentiating the synapse. Also, these signals recruit additional receptors into the post-synaptic membrane, stimulating 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. [5]

The second mechanism depends on a second messenger cascade regulating gene transcription and changes in the levels of key proteins 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. [6] 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. [7] 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 messengers. Phosphodiesterase, for example, breaks down the secondary messenger cAMP, which has been implicated in increased AMPA receptor synthesis in the post-synaptic neuron [ citation needed ].

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, spine necks are lengthened producing increased electrical isolation. [8] The end result is long-term maintenance of LTP. [9]

The number of ion channels on the post-synaptic membrane affects the strength of the synapse. [10] 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, N-methyl D-aspartate receptor (NMDA receptor) and AMPA receptors are added to the membrane by exocytosis and removed by endocytosis. [11] [12] [13] These processes, and by extension the number of receptors on the membrane, can be altered by synaptic activity. [11] [13] 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. [14] 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. [15] 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. [13] Synaptic scaling is a primary mechanism by which a neuron is able to stabilize firing rates up or down. [16]

Synaptic scaling serves to maintain the strengths of synapses relative to each other, lowering amplitudes of small excitatory postsynaptic potentials in response to continual excitation and raising them after prolonged blockage or inhibition. [13] This effect occurs gradually over hours or days, by changing the numbers of NMDA receptors 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 Ca2+ 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. [17] Synaptic scaling is a primary mechanism by which a neuron to be selective to its varying inputs. [18] 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. [19]

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. [20] Specificity is also an important aspect of CAMKII signaling involving nanodomain calcium. [7] The spatial gradient of PKA between dendritic spines and shafts is also important for the strength and regulation of synaptic plasticity. [6] 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:

  1. Change in the probability of glutamate release.
  2. Insertion or removal of post-synaptic AMPA receptors.
  3. Phosphorylation and de-phosphorylation inducing a change in AMPA receptor conductance.

Of these, the latter 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

where

Both and 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. [21]

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 an increase in the amount of packaged transmitter released in response to each action potential. [22] 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. [23] heterosynaptic depression is thought to be linked to the release of adenosine triphosphate (ATP) from astrocytes. [24]

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. [2] 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. [24] The turning point for the synaptic modification of a synapse has been found to be modifiable itself, depending on the history of the synapse. [25] Recently, a number of attempts have been made to offer a comprehensive model that could account for most forms of synaptic plasticity. [26]

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 astrocytes has been found to lead to a significant reduction of LTD in the hippocampus. [24] Activity-dependent LTD was investigated in 2011 for the electrical synapses (modification of Gap Junctions efficacy through their activity). [27] In the brain, cerebellum is one of the structures where LTD is a form of neuroplasticity. [28]

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 axonal bouton, dendritic spine and postsynaptic density. [15] On the molecular level, an increase of the postsynaptic scaffolding proteins PSD-95 and Homer1c has been shown to correlate with the stabilization of synaptic enlargement. [15]

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 astrocytes. [24] 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. [29] 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. [30]

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 cells, the most researched type being astrocytes. [24]

Computational use of plasticity

Every kind of synaptic plasticity has different computational uses. [31] Short-term facilitation has been demonstrated to serve as both working memory and mapping input for readout, short-term depression for removing auto-correlation. Long-term potentiation is used for spatial memory storage while long-term depression for both encoding space features, selective weakening of synapses and clearing old memory traces respectively. Forward spike-timing-dependent plasticity is used for long range temporal correlation, temporal coding and spatiotemporal coding. The reversed spike-timing-dependent plasticity acts as sensory filtering.

See also

Related Research Articles

<span class="mw-page-title-main">Dendritic spine</span> Small protrusion on a dendrite that receives input from a single axon

A dendritic spine is a small membrane protrusion from a neuron's dendrite that typically receives input from a single axon at the synapse. Dendritic spines serve as a storage site for synaptic strength and help transmit electrical signals to the neuron's cell body. Most spines have a bulbous head, and a thin neck that connects the head of the spine to the shaft of the dendrite. The dendrites of a single neuron can contain hundreds to thousands of spines. In addition to spines providing an anatomical substrate for memory storage and synaptic transmission, they may also serve to increase the number of possible contacts between neurons. It has also been suggested that changes in the activity of neurons have a positive effect on spine morphology.

<span class="mw-page-title-main">Long-term potentiation</span> Persistent strengthening of synapses based on recent patterns of activity

In neuroscience, long-term potentiation (LTP) is a persistent strengthening of synapses based on recent patterns of activity. These are patterns of synaptic activity that produce a long-lasting increase in signal transmission between two neurons. The opposite of LTP is long-term depression, which produces a long-lasting decrease in synaptic strength.

<span class="mw-page-title-main">AMPA receptor</span> Transmembrane protein family

The α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (also known as AMPA receptor, AMPAR, or quisqualate receptor) is an ionotropic transmembrane receptor for glutamate (iGluR) and predominantly Na+ ion channel that mediates fast synaptic transmission in the central nervous system (CNS). It has been traditionally classified as a non-NMDA-type receptor, along with the kainate receptor. Its name is derived from its ability to be activated by the artificial glutamate analog AMPA. The receptor was first named the "quisqualate receptor" by Watkins and colleagues after a naturally occurring agonist quisqualate and was only later given the label "AMPA receptor" after the selective agonist developed by Tage Honore and colleagues at the Royal Danish School of Pharmacy in Copenhagen. The GRIA2-encoded AMPA receptor ligand binding core (GluA2 LBD) was the first glutamate receptor ion channel domain to be crystallized.

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

In neuroscience, a silent synapse is an excitatory glutamatergic synapse whose postsynaptic membrane contains NMDA-type glutamate receptors but no AMPA-type glutamate receptors. These synapses are named "silent" because normal AMPA receptor-mediated signaling is not present, rendering the synapse inactive under typical conditions. Silent synapses are typically considered to be immature glutamatergic synapses. As the brain matures, the relative number of silent synapses decreases. However, recent research on hippocampal silent synapses shows that while they may indeed be a developmental landmark in the formation of a synapse, that synapses can be "silenced" by activity, even once they have acquired AMPA receptors. Thus, silence may be a state that synapses can visit many times during their lifetimes.

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The spine apparatus (SA) is a specialized form of endoplasmic reticulum (ER) that is found in a subpopulation of dendritic spines in central neurons. It was discovered by Edward George Gray in 1959 when he applied electron microscopy to fixed cortical tissue. The SA consists of a series of stacked discs that are connected to each other and to the dendritic system of ER-tubules. The actin binding protein synaptopodin is an essential component of the SA. Mice that lack the gene for synaptopodin do not form a spine apparatus. The SA is believed to play a role in synaptic plasticity, learning and memory, but the exact function of the spine apparatus is still enigmatic.

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

Nonsynaptic plasticity is a form of neuroplasticity that involves modification of ion channel function in the axon, dendrites, and cell body that results in specific changes in the integration of excitatory postsynaptic potentials and inhibitory postsynaptic potentials. Nonsynaptic plasticity is a modification of the intrinsic excitability of the neuron. It interacts with synaptic plasticity, but it is considered a separate entity from synaptic plasticity. Intrinsic modification of the electrical properties of neurons plays a role in many aspects of plasticity from homeostatic plasticity to learning and memory itself. Nonsynaptic plasticity affects synaptic integration, subthreshold propagation, spike generation, and other fundamental mechanisms of neurons at the cellular level. These individual neuronal alterations can result in changes in higher brain function, especially learning and memory. However, as an emerging field in neuroscience, much of the knowledge about nonsynaptic plasticity is uncertain and still requires further investigation to better define its role in brain function and behavior.

Synaptic tagging, or the synaptic tagging hypothesis, has been proposed to explain how neural signaling at a particular synapse creates a target for subsequent plasticity-related product (PRP) trafficking essential for sustained LTP and LTD. Although the molecular identity of the tags remains unknown, it has been established that they form as a result of high or low frequency stimulation, interact with incoming PRPs, and have a limited lifespan.

In neuroscience, synaptic scaling is a form of homeostatic plasticity, in which the brain responds to chronically elevated activity in a neural circuit with negative feedback, allowing individual neurons to reduce their overall action potential firing rate. Where Hebbian plasticity mechanisms modify neural synaptic connections selectively, synaptic scaling normalizes all neural synaptic connections by decreasing the strength of each synapse by the same factor, so that the relative synaptic weighting of each synapse is preserved.

Long-term potentiation (LTP), thought to be the cellular basis for learning and memory, involves a specific signal transmission process that underlies synaptic plasticity. Among the many mechanisms responsible for the maintenance of synaptic plasticity is the cadherin–catenin complex. By forming complexes with intracellular catenin proteins, neural cadherins (N-cadherins) serve as a link between synaptic activity and synaptic plasticity, and play important roles in the processes of learning and memory.

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<span class="mw-page-title-main">Homosynaptic plasticity</span> Type of synaptic plasticity.

Homosynaptic plasticity is one type of synaptic plasticity. Homosynaptic plasticity is input-specific, meaning changes in synapse strength occur only at post-synaptic targets specifically stimulated by a pre-synaptic target. Therefore, the spread of the signal from the pre-synaptic cell is localized.

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

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

References

  1. ↑ Hughes JR (January 1958). "Post-tetanic potentiation". Physiological Reviews. 38 (1): 91–113. doi:10.1152/physrev.1958.38.1.91. PMID   13505117.
  2. 1 2 3 Gerrow K, Triller A (October 2010). "Synaptic stability and plasticity in a floating world". Current Opinion in Neurobiology. 20 (5): 631–9. doi:10.1016/j.conb.2010.06.010. PMID   20655734. S2CID   7988672.
  3. ↑ Gaiarsa JL, Caillard O, Ben-Ari Y (November 2002). "Long-term plasticity at GABAergic and glycinergic synapses: mechanisms and functional significance". Trends in Neurosciences. 25 (11): 564–70. doi:10.1016/S0166-2236(02)02269-5. PMID   12392931. S2CID   17365083.
  4. ↑ Bear MF, Connors BW, and Paradisio MA. 2007. Neuroscience: Exploring the Brain, 3rd ed. Lippincott, Williams & Wilkins
  5. ↑ Soderling TR, Derkach VA (February 2000). "Postsynaptic protein phosphorylation and LTP". Trends in Neurosciences. 23 (2): 75–80. doi:10.1016/S0166-2236(99)01490-3. PMID   10652548. S2CID   16733526.
  6. 1 2 Zhong H, Sia GM, Sato TR, Gray NW, Mao T, Khuchua Z, et al. (May 2009). "Subcellular dynamics of type II PKA in neurons". Neuron. 62 (3): 363–74. doi:10.1016/j.neuron.2009.03.013. PMC   2702487 . PMID   19447092.
  7. 1 2 Lee SJ, Escobedo-Lozoya Y, Szatmari EM, Yasuda R (March 2009). "Activation of CaMKII in single dendritic spines during long-term potentiation". Nature. 458 (7236): 299–304. Bibcode:2009Natur.458..299L. doi:10.1038/nature07842. PMC   2719773 . PMID   19295602.
  8. ↑ Araya R, Jiang J, Eisenthal KB, Yuste R (November 2006). "The spine neck filters membrane potentials". Proceedings of the National Academy of Sciences of the United States of America. 103 (47): 17961–6. Bibcode:2006PNAS..10317961A. doi: 10.1073/pnas.0608755103 . PMC   1693855 . PMID   17093040.
  9. ↑ Shoji-Kasai Y, Ageta H, Hasegawa Y, Tsuchida K, Sugino H, Inokuchi K (November 2007). "Activin increases the number of synaptic contacts and the length of dendritic spine necks by modulating spinal actin dynamics". Journal of Cell Science. 120 (Pt 21): 3830–7. doi: 10.1242/jcs.012450 . PMID   17940062.
  10. ↑ Debanne D, Daoudal G, Sourdet V, Russier M (2003). "Brain plasticity and ion channels". Journal of Physiology, Paris. 97 (4–6): 403–14. doi:10.1016/j.jphysparis.2004.01.004. PMID   15242652. S2CID   19116187.
  11. 1 2 Shi SH, Hayashi Y, Petralia RS, Zaman SH, Wenthold RJ, Svoboda K, Malinow R (June 1999). "Rapid spine delivery and redistribution of AMPA receptors after synaptic NMDA receptor activation". Science. 284 (5421): 1811–6. CiteSeerX   10.1.1.376.3281 . doi:10.1126/science.284.5421.1811. PMID   10364548.
  12. ↑ Song I, Huganir RL (November 2002). "Regulation of AMPA receptors during synaptic plasticity". Trends in Neurosciences. 25 (11): 578–88. doi:10.1016/S0166-2236(02)02270-1. PMID   12392933. S2CID   1993509.
  13. 1 2 3 4 Pérez-Otaño I, Ehlers MD (May 2005). "Homeostatic plasticity and NMDA receptor trafficking" (PDF). Trends in Neurosciences. 28 (5): 229–38. doi:10.1016/j.tins.2005.03.004. PMID   15866197. S2CID   22901201. Archived from the original (PDF) on July 20, 2011. Retrieved 2007-06-08.
  14. ↑ Bear MF (2007). Neuroscience: Exploring the Brain . Third Edition. Lippincott Williams & Wilkins. pp.  779. ISBN   978-0-7817-6003-4.
  15. 1 2 3 Meyer D, Bonhoeffer T, Scheuss V (April 2014). "Balance and stability of synaptic structures during synaptic plasticity". Neuron. 82 (2): 430–43. doi: 10.1016/j.neuron.2014.02.031 . PMID   24742464.
  16. ↑ Desai NS, Cudmore RH, Nelson SB, Turrigiano GG (August 2002). "Critical periods for experience-dependent synaptic scaling in visual cortex". Nature Neuroscience. 5 (8): 783–9. doi:10.1038/nn878. PMID   12080341. S2CID   17747903.
  17. ↑ Abraham WC, Tate WP (July 1997). "Metaplasticity: a new vista across the field of synaptic plasticity". Progress in Neurobiology. 52 (4): 303–23. doi:10.1016/S0301-0082(97)00018-X. PMID   9247968. S2CID   33285995.
  18. ↑ Abbott LF, Nelson SB (November 2000). "Synaptic plasticity: taming the beast". Nature Neuroscience. 3 Suppl: 1178–83. doi:10.1038/81453. PMID   11127835. S2CID   2048100.
  19. ↑ Cooper SJ (January 2005). "Donald O. Hebb's synapse and learning rule: a history and commentary". Neuroscience and Biobehavioral Reviews. 28 (8): 851–74. doi:10.1016/j.neubiorev.2004.09.009. PMID   15642626. S2CID   40805686.
  20. ↑ Kennedy MJ, Davison IG, Robinson CG, Ehlers MD (April 2010). "Syntaxin-4 defines a domain for activity-dependent exocytosis in dendritic spines". Cell. 141 (3): 524–35. doi:10.1016/j.cell.2010.02.042. PMC   2874581 . PMID   20434989.
  21. ↑ Shouval HZ, Castellani GC, Blais BS, Yeung LC, Cooper LN (December 2002). "Converging evidence for a simplified biophysical model of synaptic plasticity" (PDF). Biological Cybernetics. 87 (5–6): 383–91. doi:10.1007/s00422-002-0362-x. PMID   12461628. S2CID   7753630.
  22. ↑ Stevens CF, Wesseling JF (January 1999). "Augmentation is a potentiation of the exocytotic process". Neuron. 22 (1): 139–46. doi: 10.1016/S0896-6273(00)80685-6 . PMID   10027296.
  23. ↑ Zucker RS, Regehr WG (Mar 2002). "Short-term synaptic plasticity". Annual Review of Physiology. 64: 355–405. doi:10.1146/annurev.physiol.64.092501.114547. PMID   11826273. S2CID   7980969.
  24. 1 2 3 4 5 Ben Achour S, Pascual O (November 2010). "Glia: the many ways to modulate synaptic plasticity". Neurochemistry International. 57 (4): 440–5. doi:10.1016/j.neuint.2010.02.013. PMID   20193723. S2CID   1718772.
  25. ↑ Bear MF (July 1995). "Mechanism for a sliding synaptic modification threshold". Neuron. 15 (1): 1–4. doi: 10.1016/0896-6273(95)90056-x . PMID   7619513.
  26. ↑ Michmizos D, Koutsouraki E, Asprodini E, Baloyannis S (June 2011). "Synaptic plasticity: a unifying model to address some persisting questions". The International Journal of Neuroscience. 121 (6): 289–304. doi:10.3109/00207454.2011.556283. PMID   21348800. S2CID   24610392.
  27. ↑ Haas JS, Zavala B, Landisman CE (October 2011). "Activity-dependent long-term depression of electrical synapses". Science. 334 (6054): 389–93. Bibcode:2011Sci...334..389H. doi:10.1126/science.1207502. PMC   10921920 . PMID   22021860. S2CID   35398480.
  28. ↑ Mitoma H, Kakei S, Yamaguchi K, Manto M (April 2021). "Physiology of Cerebellar Reserve: Redundancy and Plasticity of a Modular Machine". Int. J. Mol. Sci. 22 (9): 4777. doi: 10.3390/ijms22094777 . PMC   8124536 . PMID   33946358.
  29. ↑ Artola A, Singer W (November 1993). "Long-term depression of excitatory synaptic transmission and its relationship to long-term potentiation". Trends in Neurosciences. 16 (11): 480–7. doi:10.1016/0166-2236(93)90081-V. PMID   7507622. S2CID   3974242.
  30. ↑ Tazerart S, Mitchell DE, Miranda-Rottmann S, Araya R (August 2020). "A spike-timing-dependent plasticity rule for dendritic spines". Nature Communications. 11 (1): 4276. Bibcode:2020NatCo..11.4276T. doi:10.1038/s41467-020-17861-7. PMC   7449969 . PMID   32848151.
  31. ↑ Prati E (2016). "Atomic scale nanoelectronics for quantum neuromorphic devices: comparing different materials". International Journal of Nanotechnology. 13 (7): 509–523. arXiv: 1606.01884 . Bibcode:2016IJNT...13..509P. doi:10.1504/IJNT.2016.078543. S2CID   18697109.

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