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necessity for the induction of long-term depression. There are several sources of calcium signaling that elicit LTD: climbing fibres and parallel fibres which converge onto
Purkinje cells. Calcium signaling in the post-synaptic cell involved both spatial and temporal overlap of climbing fibre induced calcium release into dendrites as well as parallel fibre induced mGluRs and IP3 mediated calcium release. In the climbing fibres, AMPAR-mediated depolarization induces a regenerative action potential that spreads to the dendrites, which is generated by voltage-gated calcium channels. Paired with PF-mediated mGluR1 activation results in LTD induction. In the parallel fibres, GluRs are activated by constant activation of the parallel fibres which indirectly induces the IP3 to bind to its receptor (IP3) and activate calcium release from intracellular storage. In calcium induction, there is a positive feedback loop to regenerate calcium for long-term depression. Climbing and parallel fibres must be activated together to depolarize the Purkinje cells while activating mGlur1s. Timing is a critical component to CF and PF as well, a better calcium release involves PF activation a few hundred milliseconds before CF activity.
177:. Homosynaptic LTD is restricted to the individual synapse that is activated by a low frequency stimulus. In other words, this form of LTD is activity-dependent, because the events causing the synaptic weakening occur at the same synapse that is being activated. Homosynaptic LTD is also associative in that it correlates the activation of the postsynaptic neuron with the firing of the presynaptic neuron. Heterosynaptic LTD, in contrast, occurs at synapses that are not potentiated or are inactive. The weakening of a synapse is independent of the activity of the presynaptic or postsynaptic neurons as a result of the firing of a distinct modulatory interneuron. Thus, this form of LTD impacts synapses nearby those receiving
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other, MAPKKK dual phosphorylates MAPKK and in turn dual phosphorylates MAPK. There is a positive feedback loop that results from a simultaneous input of signals from PF-CF and increases DAG and Ca in
Purkinje dendritic spines. Calcium and DAG activate conventional PKC (cPKC), which then activates MAPKKK and the rest of the MAPK cascade. Activated MAPK and Ca activate PLA2, AA and cPKC creating a positive feedback loop. Induced cPKC phosphorylates AMPA receptors and are eventually removed from the postsynaptic membrane via endocytosis. The timescale is for this process is approximately 40 minutes. Overall, the magnitude of the LTD correlates with AMPAR phosphorylation.
295:) activation (which is accomplished jointly by calcium and DAG). PKC phosphorylates AMPA receptors, which promotes their dissociation from scaffold proteins in the post-synaptic membrane and subsequent internalization. With the loss of AMPA receptors, the postsynaptic Purkinje cell response to glutamate release from parallel fibers is depressed. Calcium triggering in the cerebellum is a critical mechanism involved in long-term depression. Parallel fibre terminals and climbing fibres work together in a positive feedback loop for invoking high calcium release. LTD is involved in predictive control exerted by cerebellar circuitry and cerebellar reserve.
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161:(BCM model) proposes that a certain threshold exists such that a level of postsynaptic response below the threshold leads to LTD and above it leads to LTP. BCM theory further proposes that the level of this threshold depends upon the average amount of postsynaptic activity. Scaling has been found to occur when the strength of all of a neuron’s excitatory inputs are scaled up or down. LTD and LTP coincide with metaplasticity and synaptic scaling to maintain proper neuronal network function.
263:. LTD decreases the efficacy of parallel fiber synapse transmission, though, according to recent findings, it also impairs climbing fiber synapse transmission. Both parallel fibers and climbing fibers must be simultaneously activated for LTD to occur. With respect to calcium release however, it is best if the parallel fibers are activated a few hundred milliseconds before the climbing fibres. In one pathway, parallel fiber terminals release glutamate to activate
228:, which subsequently phosphorylate target proteins, LTD arises from activation of calcium-dependent phosphatases that dephosphorylate the target proteins. Selective activation of these phosphatases by varying calcium levels might be responsible for the different effects of calcium observed during LTD. The activation of postsynaptic phosphatases causes internalization of synaptic AMPA receptors (also a type of iGluRs) into the postsynaptic cell by
475:. The serotonin system in the PFC plays an important role in regulating cognition and emotion. Serotonin, in cooperation with a group I metabotropic glutamate receptor (mGluR) agonist, facilitates LTD induction through augmentation of AMPA receptor internalization. This mechanism possibly underlies serotonin's role in the control of cognitive and emotional processes that synaptic plasticity in PFC neurons mediates.
621:. Cerebellar LTD is thought to lead to motor learning, and hippocampal LTD is thought to contribute to the decay of memory. However, recent studies have found that hippocampal LTD may not act as the reverse of LTP, but may instead contribute to spatial memory formation. Although LTD is now well characterized, these hypotheses about its contribution to motor learning and memory remain controversial.
57:(LTP), LTD is one of several processes that serves to selectively weaken specific synapses in order to make constructive use of synaptic strengthening caused by LTP. This is necessary because, if allowed to continue increasing in strength, synapses would ultimately reach a ceiling level of efficiency, which would inhibit the encoding of new information. Both LTD and LTP are forms of
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synaptic failure in AD and in types of age-related Aβ accumulation. This research provides a novel understanding of the development of AD and proposes potential therapeutic targets for the disease. Further research is needed to understand how soluble amyloid beta protein specifically interferes with glutamate transporters.
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New evidence suggests that LTP works to encode space, whereas LTD works to encode the features of space. Specifically, it is accepted that encoding of experience takes place on a hierarchy. Encoding of new space is the priority of LTP, while information about orientation in space could be encoded by
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was observed. After the rats were brought back to their initial environment, LTD activity was lost. It was found that if the rats were exposed to novelty, the electrical stimulation required to depress synaptic transmission was of lower frequency than without novelty. When the rat was put in a novel
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When postsynaptic action potential firing occurs prior to presynaptic afferent firing, both presynaptic endocannabinoid (CB1) receptors and NMDA receptors are stimulated at the same time. Postsynaptic spiking alleviates the Mg block on NMDA receptors. The postsynaptic depolarization will subside by
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as well as in the stratum radiatum of the hippocampus. Additionally, endocannabinoids play an important role in regulating various forms of synaptic plasticity. They are involved in inhibition of LTD at parallel fiber
Purkinje neuron synapses in the cerebellum and NMDA receptor-dependent LTD in the
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Further research has determined calcium's role in long-term depression induction. While other mechanisms of long-term depression are being investigated, calcium's role in LTD is a defined and well understood mechanism by scientists. High calcium concentrations in the post-synaptic
Purkinje cells is a
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LTD in the hippocampus and cerebellum have been the best characterized, but there are other brain areas in which mechanisms of LTD are understood. LTD has also been found to occur in different types of neurons that release various neurotransmitters, however, the most common neurotransmitter involved
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In the field of research of cerebellum disorders, auto-antigens are involved in molecular cascades for induction of LTD of synaptic transmissions between parallel fibers (PFs) and
Purkinje cells (PCs), a mechanism of synaptic plasticity in the cerebellum. Anti-VGCC, anti-mGluR1, and anti-GluR delta
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The magnitude of this LTD is comparable to that which results from low frequency stimulation, but with fewer stimulation pulses (40 PPS for 900 low frequency stimulations). It is suggested that the effect of NE is to control the gain of NMDA receptor-dependent homosynaptic LTD. Like norepinephrine,
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the back-propagating action potential. There is a plasticity window: if the presynaptic and postsynaptic spikes are too far apart (i.e., more than 15 ms apart), there is little chance of plasticity. The possible window for LTD is wider than that for LTP – although it is important to note that this
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occurs. NMDA-receptor dependent LTD is induced by moderate rises in postsynaptic calcium levels. When Ca entry is below threshold, it leads to LTD. The threshold level in area CA1 is on a sliding scale that depends on the history of the synapse. If the synapse has already been subject to LTP, the
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and the CA1 pyramidal cells. LTD at the
Schaffer collateral-CA1 synapses depends on the timing and frequency of calcium influx. LTD occurs at these synapses when Schaffer collaterals are stimulated repetitively for extended time periods (10–15 minutes) at a low frequency (approximately 1 Hz).
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There is a series of signaling cascades, MAPK, in the cerebellum that plays a critical role in cerebellum LTD. The MAPK cascade is important in information processing within neurons and other various types of cells. The cascade includes MAPKKK, MAPKK, and MAPK. Each is dual phosphorylated by the
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recycling at hippocampal synapses. Excess glutamate is a proposed contributor to the progressive neuronal loss involved in AD. Evidence that soluble Aβ enhances LTD through a mechanism involving altered glutamate uptake at hippocampal synapses has important implications for the initiation of
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is prevented by (1R-1-benzo thiophen-5-yl-2 ethanol hydrochloride (T-588). Likewise, LTD in mice was disrupted using several experimental techniques with no observable deficits in motor learning or performance. These taken together suggest that the correlation between cerebellar LTD and motor
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mutant mice maintained a normal cerebellar anatomy but had weak LTD and consequently impaired motor learning. However the relationship between cerebellar LTD and motor learning has been seriously challenged. A study on rats and mice proved that normal motor learning occurs while LTD of
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Abs-associated cerebellar ataxias share one common pathophysiological mechanism: a deregulation in PF-PC LTD. This causes an impairment of restoration or maintenance of the internal model hold by the cerebellum and triggers cerebellar ataxias. These diseases are LTDpathies.
826:-LTD(A) contributes to the elimination of excess synapses during development. This process is downregulated after synapses have stabilized, and is regulated by GSK3β. During neurodegeneration, there is the possibility that there is deregulation of GSK3β resulting in '
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blocking experiments. It is proposed that there are multiple memory mechanisms in the perirhinal cortex. The exact mechanisms are not completely understood, however pieces of the mechanisms have been deciphered. Studies suggest that one
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glutamate receptors (iGluRs), is required for calcium entry into the CA1 postsynaptic cell. Change in voltage provides a graded control of postsynaptic Ca by regulating NMDAR-dependent Ca influx, which is responsible for initiating LTD.
105:(LTP) is the opposing process to LTD; it is the long-lasting increase of synaptic strength. In conjunction, LTD and LTP are factors affecting neuronal synaptic plasticity. LTD is thought to result mainly from a decrease in postsynaptic
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the time an EPSP occurs, enabling Mg to return to its inhibitory binding site. Thus, the influx of Ca in the postsynaptic cell is reduced. CB1 receptors detect postsynaptic activity levels via retrograde endocannabinoid release.
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is ongoing. It has been suggested that a reduction in NMDAR-dependent LTD may be due to changes not only in postsynaptic AMPARs but also in NMDARs, and these changes are perhaps present in early and mild forms of
Alzheimer-type
291:, raising intracellular calcium levels. Together, DAG and IP3 augment the calcium concentration rise by targeting IP3-sensitive receptors triggering release of calcium from intracellular stores as well as protein kinase C (
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with the synaptic injury and memory loss related to AD. While Aβ's role in LTD regulation has not been clearly understood, it has been found that soluble Aβ facilitates hippocampal LTD and is mediated by a decrease in
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diseases research remains inconclusive as to the mechanisms that triggers the degeneration in the brain. New evidence demonstrates there are similarities between the apoptotic pathway and LTD which involves the
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affect long-lasting plasticity processes in various parts of the brain, serving both as regulators of pathways and necessary retrograde messengers in specific forms of LTD. In regard to retrograde signaling,
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glutamate receptors in the postsynaptic
Purkinje cell. When glutamate binds to the AMPA receptor, the membrane depolarizes. Glutamate binding to the metabotropic receptor activates phospholipase C (
113:. However, it is likely that other plasticity mechanisms play a role as well. Hippocampal LTD may be important for the clearing of old memory traces. Hippocampal/cortical LTD can be dependent on
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Aiba A, Kano M, Chen C, Stanton ME, Fox GD, Herrup K, Zwingman TA, Tonegawa S (October 1994). "Deficient cerebellar long-term depression and impaired motor learning in mGluR1 mutant mice".
145:, they would eventually come to the point of complete inactivity or too much activity. To prevent neurons from becoming static, there are two regulatory forms of plasticity that provide
428:. LTD has also been found to occur in this fashion in layer II. A different mechanism is at work in the LTD that occurs in layer V. In layer V, LTD requires low frequency stimulation,
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Min SS, Quan HY, Ma J, Lee KH, Back SK, Na HS, Han SH, Yee JY, Kim C, Han JS, Seol GH (May 2009). "Impairment of long-term depression induced by chronic brain inflammation in rats".
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threshold is raised, increasing the probability that a calcium influx will yield LTD. In this way, a "negative feedback" system maintains synaptic plasticity. Activation of
125:. The result of the underlying-LTD molecular mechanism in cerebellum is the phosphorylation of AMPA glutamate receptors and their elimination from the surface of the
368:, with postsynaptic depolarization and increased postsynaptic calcium influx. The second is initiated by a high frequency stimulus and is arbitrated by presynaptic
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Schonewille M, Gao Z, Boele HJ, Veloz MF, Amerika WE, Simek AA, De Jeu MT, Steinberg JP, Takamiya K, Hoebeek FE, Linden DJ, Huganir RL, De Zeeuw CI (April 2011).
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in which a millisecond-scale change in the timing of presynaptic and postsynaptic spikes will cause differences in postsynaptic Ca signals, inducing either
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is thought to occur through the same mechanism as NMDAR-dependent LTD, because this form of plasticity is reduced after cocaine use. After, the amount of
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experiments "in vivo" indicate that post-leading-pre spike delays elicit synaptic depression. LTP is induced when neurotransmitter release occurs 5-15 ms
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of the visual cortex causes LTD in layer III. In this form of LTD, low-frequency stimulation of one pathway results in LTD only for that input, making it
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STDP selectively enhances and consolidates specific synaptic modifications (signals), while depressing global ones (noise). This results in a sharpened
1343:
Turrigiano GG, Leslie KR, Desai NS, Rutherford LC, Nelson SB (February 1998). "Activity-dependent scaling of quantal amplitude in neocortical neurons".
830:'. If there is excess removal of synapses, this illustrates early signs of neurodegeration and a link between apoptosis and neurodegeneration diseases.
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is proposed to control the gain of NMDA receptor-dependent homosynaptic LTD, but it is likely to be a promoter of additional LTD mechanisms as well.
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density, although a decrease in presynaptic neurotransmitter release may also play a role. Cerebellar LTD has been hypothesized to be important for
1929:"Serotonin facilitates long-term depression induction in prefrontal cortex via p38 MAPK/Rab5-mediated enhancement of AMPA receptor internalization"
1397:
Escobar ML, Derrick B (2007). "Long-Term
Potentiation and Depression as Putative Mechanisms for Memory Formation". In Bermudez-Rattoni F (ed.).
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Manahan-Vaughan D (2005). "Hippocampal Long-Term
Depression as a Declarative Memory Mechanism". In Scharfman HE, Stanton PK, Bramham C (eds.).
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result from this particular stimulation pattern. The magnitude of calcium signal in the postsynaptic cell largely determines whether LTD or
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Markram H, Lübke J, Frotscher M, Sakmann B (January 1997). "Regulation of synaptic efficacy by coincidence of postsynaptic APs and EPSPs".
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The mechanism of long-term depression has been well characterized in limited parts of the brain. However, the way in which LTD affects
1620:"Dopaminergic control of corticostriatal long-term synaptic depression in medium spiny neurons is mediated by cholinergic interneurons"
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LTD has been correlated with spatial learning in rats, and it is crucial in forming a complete spatial map. It suggested that LTD and
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function widely throughout the brain in presynaptic inhibition. Endocannabinoid retrograde signaling has been shown to effect LTD at
2122:"Synaptic modifications in cultured hippocampal neurons: dependence on spike timing, synaptic strength, and postsynaptic cell type"
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and repetitive stimulation of glutamatergic fibers (13 Hz for ten minutes), resulting in a long-term decrease in presynaptic
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and scaling. Metaplasticity is expressed as a change in the capacity to provoke subsequent synaptic plasticity, including LTD and
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Kemp A, Manahan-Vaughan D (March 2007). "Hippocampal long-term depression: master or minion in declarative memory processes?".
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2725:"Soluble oligomers of amyloid β-protein facilitate hippocampal long-term depression by disrupting neuronal glutamate uptake"
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It has been found that paired-pulse stimulation (PPS) induces a form of homosynaptic LTD in the superficial layers of the
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release. It is proposed that LTD in GABAergic striatal neurons leads to a long-term decrease in inhibitory effects on the
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It is highly important for neurons to maintain a variable range of neuronal output. If synapses were only reinforced by
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in human cortical networks that facilitates the detection of relevant signals during information processing in humans.
1296:"Theory for the development of neuron selectivity: orientation specificity and binocular interaction in visual cortex"
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1084:"Bidirectional regulation of hippocampal long-term synaptic plasticity and its influence on opposing forms of memory"
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is still not well understood. Determining this relationship is presently one of the major focuses of LTD research.
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Malleret G, Alarcon JM, Martel G, Takizawa S, Vronskaya S, Yin D, Chen IZ, Kandel ER, Shumyatsky GP (Mar 2010).
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Massey PV, Bashir ZI (April 2007). "Long-term depression: multiple forms and implications for brain function".
1720:"Group 1 mGluR-dependent synaptic long-term depression: mechanisms and implications for circuitry and disease"
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552:. Endocannabinoids are implicated in LTD of inhibitory inputs (LTDi) within the basolateral nucleus of the
287:. In the pathway initiated by activation of climbing fibers, calcium enters the postsynaptic cell through
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Computational models predict that LTD creates a gain in recognition memory storage capacity over that of
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Additionally, researchers have recently discovered a new mechanism (which involves LTD) linking soluble
2774:"Cerebellar long-term depression and autoimmune target of auto-antibodies: the concept of LTDpathies"
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Blanke ML, VanDongen AM (2008). "Activation Mechanisms of the NMDA Receptor". In VanDongen AM (ed.).
1476:"Mechanisms underlying induction of homosynaptic long-term depression in area CA1 of the hippocampus"
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or LTD. LTD occurs when postsynaptic spikes precede presynaptic spikes by up to 20-50 ms. Whole-cell
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Welsh JP, Yamaguchi H, Zeng XH, Kojo M, Nakada Y, Takagi A, Sugimori M, Llinás RR (November 2005).
217:
2171:"Timing-based LTP and LTD at vertical inputs to layer II/III pyramidal cells in rat barrel cortex"
1880:"Modulation of long-term synaptic depression in visual cortex by acetylcholine and norepinephrine"
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mechanisms, thereby reducing sensitivity to glutamate released by Schaffer collateral terminals.
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106:
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Collingridge GL, Peineau S, Howland JG, Wang YT (July 2010). "Long-term depression in the CNS".
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by a high frequency stimulus coupled with postsynaptic depolarization, coactivation of dopamine
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3183:
3127:
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2438:"Normal motor learning during pharmacological prevention of Purkinje cell long-term depression"
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Nicholls RE, Alarcon JM, Malleret G, Carroll RC, Grody M, Vronskaya S, Kandel ER (April 2008).
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424:, because it is triggered by a small elevation in postsynaptic calcium ions and activation of
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Pérez-Otaño I, Ehlers MD (May 2005). "Homeostatic plasticity and NMDA receptor trafficking".
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causes a hyperexcitability in the NAc neurons (GABAergic MSNs). This leads to an increase of
602:
569:) refers to the timing of presynaptic and postsynaptic action potentials. STDP is a form of
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lasting hours or longer following a long patterned stimulus. LTD occurs in many areas of the
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Studies have connected deficient cerebellar LTD with impaired motor learning. In one study,
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Abraham WC, Bear MF (April 1996). "Metaplasticity: the plasticity of synaptic plasticity".
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8:
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58:
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1035:"Transgenic mice lacking NMDAR-dependent LTD exhibit deficits in behavioral flexibility"
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360:, three forms or LTD have been established. The mechanism of the first is similar to
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2030:"Spike Timing-Dependent Synaptic Depression in the In Vivo Barrel Cortex of the Rat"
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Long-term depression has long been hypothesized to be an important mechanism behind
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Duguid IC, Smart TG (2008). "Presynaptic NMDA Receptors". In VanDongen AM (ed.).
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1769:"Mechanisms of synaptic depression triggered by metabotropic glutamate receptors"
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with varying mechanisms depending upon brain region and developmental progress.
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24:
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in LTD is L-glutamate. L-glutamate acts on the N-methyl-D- aspartate receptors (
3254:
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2253:"Focusing effect of acetylcholine on neuroplasticity in the human motor cortex"
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neurons in the VTA less likely to fire, and thus resulting in the symptoms of
412:. Recurring low-frequency stimulation of layer IV of the visual cortex or the
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737:. This is possibly due to homeostatic synaptic scaling. This increase in
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Li S, Hong S, Shepardson NE, Walsh DM, Shankar GM, Selkoe D (June 2009).
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Wang Z, Kai L, Day M, Ronesi J, Yin HH, Ding J, Tkatch T, Lovinger DM,
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1978:"Emerging roles for endocannabinoids in long-term synaptic plasticity"
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Jacob V, Brasier DJ, Erchova I, Feldman D, Shulz DE (February 2007).
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74:), α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptors (
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1169:"Systems biology perspectives on cerebellar long-term depression"
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2 or 3, resulting in a long term reduction in the involvement of
255:, which receive two forms of excitatory input, one from a single
87:
43:
42:) is an activity-dependent reduction in the efficacy of neuronal
2891:"Activity-dependent long-term depression of electrical synapses"
1878:
Kirkwood A, Rozas C, Kirkwood J, Perez F, Bear MF (March 1999).
693:, and the finer details of space could be encoded by LTD in the
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at a much earlier time, about 20 to 30 minutes after stimulus.
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Research on the role of LTD in neurological disorders such as
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645:. In one study, rats were exposed to a novel environment, and
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24 hours after the stimulus. The other LTD mechanism involves
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Kuo MF, Grosch J, Fregni F, Paulus W, Nitsche MA (Dec 2007).
1139:. Hagerstwon, MD: Lippincott Williams & Wilkins. p.
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1012:(4th ed.). Sunderland, Mass: Sinauer. pp. 197–200.
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work together to encode different aspects of spatial memory.
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2311:"Homosynaptic long-term depression: A mechanism for memory?"
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364:-LTD: a low frequency stimulus induces LTD by activation of
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A model for the mechanisms of depotentiation and de novo LTD
2772:
Mitoma H, Honnorat J, Yamaguchi K, Manto M (January 2021).
2497:"Reevaluating the role of LTD in cerebellar motor learning"
1564:"Bidirectional synaptic plasticity: from theory to reality"
742:
2027:
1877:
637:
Studies on rats have made a connection between LTD in the
589:, whereas LTD is induced when the stimulus occurs 5-15 ms
321:
The mechanisms of LTD differ in the two subregions of the
97:) or from persistent weak synaptic stimulation (as in the
1667:
Mitoma H, Honnorat J, Yamaguchi K, Manto M (March 2021).
1427:"Mechanism for a sliding synaptic modification threshold"
1399:
Neural plasticity and memory: from genes to brain imaging
432:
signaling, and activation of presynaptic NR2B-containing
2494:
2370:
Motor learning and synaptic plasticity in the cerebellum
2220:
Biology of the NMDA Receptor (Frontiers in Neuroscience)
1824:"Homosynaptic long-term depression in the visual cortex"
1531:
Biology of the NMDA Receptor (Frontiers in Neuroscience)
2435:
1293:
2722:
2250:
3038:
1766:
1294:
Bienenstock EL, Cooper LN, Munro PW (January 1982).
560:
2950:"Neuroscience. The strength of electrical synapses"
2888:
2548:
2392:
1474:Mulkey, Rosel M.; Malenka, Robert C. (1992-11-01).
1130:
420:. This type of LTD is similar to that found in the
404:Long-term depression has also been observed in the
2590:
2588:
1166:
1132:
184:
2594:
2361:
1767:Bellone C, Lüscher C, Mameli M (September 2008).
1522:
1207:
3271:
2889:Haas JS, Zavala B, Landisman CE (October 2011).
1975:
1613:
1124:
713:(NAc). After chronic cocaine use, the amount of
169:Long-term depression can be described as either
2597:Synaptic plasticity and transsynaptic signaling
2585:
2367:
2304:
2302:
2300:
2298:
2296:
2023:
2021:
1528:
1927:Zhong P, Liu W, Gu Z, Yan Z (September 2008).
1420:
1418:
1396:
1162:
1160:
947:
945:
943:
941:
939:
937:
224:While LTP is in part due to the activation of
3024:
2634:
2632:
2630:
2628:
2626:
2624:
2372:. Cambridge, UK: Cambridge University Press.
2244:
1926:
1473:
935:
933:
931:
929:
927:
925:
923:
921:
919:
917:
2816:
2716:
2687:
2681:
2638:
2488:
2429:
2293:
2162:
2018:
1969:
1920:
1821:
1760:
1717:
1711:
1609:
1607:
1555:
1467:
1075:
1026:
951:
608:
2869:
2386:
2217:
2113:
2070:
1873:
1871:
1869:
1867:
1817:
1815:
1813:
1660:
1415:
1336:
1250:
1201:
1157:
745:release by projections from the NAc to the
701:Cocaine as a model of LTD in drug addiction
519:
396:, influencing the storage of motor skills.
3031:
3017:
2621:
2168:
1976:Gerdeman GL, Lovinger DM (November 2003).
1287:
1244:
914:
205:excitatory postsynaptic potentials (EPSPs)
3001:at the U.S. National Library of Medicine
2973:
2922:
2799:
2789:
2748:
2656:
2520:
2471:
2461:
2344:
2334:
2276:
2186:
2145:
2053:
2001:
1952:
1903:
1847:
1743:
1694:
1684:
1635:
1604:
1587:
1442:
1319:
1184:
1131:Paradiso MA, Bear MF, Connors BW (2007).
1107:
1050:
82:), and metabotropic glutamate receptors (
1864:
1810:
1568:Philos. Trans. R. Soc. Lond. B Biol. Sci
1392:
1390:
1007:
670:. Therefore, it has been concluded that
540:synapses in the prelimbic cortex of the
380:release. The third form of LTD requires
307:
234:
86:) during LTD. It can result from strong
2947:
2544:
2542:
2540:
2308:
1561:
1424:
733:is ramped up in the NAc neurons during
594:threshold depends on synaptic history.
408:, and it is proposed to be involved in
164:
3272:
2639:Kauer JA, Malenka RC (November 2007).
2599:. Berlin: Springer. pp. 305–319.
1669:"LTDpathies: a novel clinical concept"
491:, and this prediction is confirmed by
259:and one from hundreds of thousands of
3012:
2119:
1718:Lüscher C, Huber KM (February 2010).
1387:
1167:Ogasawara H, Doi T, Kawato M (2008).
1003:
1001:
999:
997:
995:
993:
991:
325:. LTD is induced at corticostriatal
136:
2537:
2368:Harnad SR, Cordo P, Bell CC (1997).
805:
478:
471:is involved in LTD induction in the
462:
2874:. New York: Springer. p. 574.
2641:"Synaptic plasticity and addiction"
760:
725:in the NAc shell. This decrease in
565:Spike timing-dependent plasticity (
298:
159:Bienenstock, Cooper and Munro model
64:
13:
2862:
2138:10.1523/JNEUROSCI.18-24-10464.1998
1896:10.1523/JNEUROSCI.19-05-01599.1999
1840:10.1523/JNEUROSCI.14-05-03404.1994
1312:10.1523/JNEUROSCI.02-01-00032.1982
988:
14:
3301:
2992:
1135:Neuroscience: exploring the brain
881:Spike timing dependent plasticity
870:Inhibitory postsynaptic potential
860:Excitatory postsynaptic potential
634:learning may have been illusory.
626:metabotropic glutamate receptor 1
561:Spike timing-dependent plasticity
3072:Lateralization of brain function
1822:Kirkwood A, Bear MF (May 1994).
399:
119:metabotropic glutamate receptors
3143:Somatosensory evoked potentials
2765:
2211:
2120:Bi GQ, Poo MM (December 1998).
443:when the synapse is exposed to
356:In the prelimbic cortex of the
275:) and produces diacylglycerol (
185:Mechanisms that weaken synapses
2269:10.1523/JNEUROSCI.4104-07.2007
2046:10.1523/JNEUROSCI.4264-06.2007
1100:10.1523/JNEUROSCI.1330-09.2010
189:
90:stimulation (as occurs in the
1:
2999:Long-Term+Synaptic+Depression
2690:Biochem. Biophys. Res. Commun
2188:10.1016/S0896-6273(00)00008-8
1265:10.1016/S0166-2236(96)80018-X
908:
544:, and it is also involved in
279:) and inositol triphosphate (
243:
216:, which belong to a class of
214:NMDA-type glutamate receptors
2741:10.1016/j.neuron.2009.05.012
2513:10.1016/j.neuron.2011.02.044
2442:Proc. Natl. Acad. Sci. U.S.A
2407:10.1016/0092-8674(94)90205-4
2315:Proc. Natl. Acad. Sci. U.S.A
2091:10.1126/science.275.5297.213
1945:10.1113/jphysiol.2008.155143
1736:10.1016/j.neuron.2010.01.016
1637:10.1016/j.neuron.2006.04.010
1492:10.1016/0896-6273(92)90248-C
1444:10.1016/0896-6273(95)90056-X
1052:10.1016/j.neuron.2008.01.039
709:is believed to occur in the
23:, a mental disorder, or the
7:
2870:Harris AL, Locke D (2009).
2257:The Journal of Neuroscience
903:Actin remodeling of neurons
833:
666:fiber, resulting in LTD in
316:
230:clathrin-coated endocytosis
53:As the opposing process to
10:
3306:
2948:Hestrin S (October 2011).
2791:10.1186/s43556-020-00024-x
2702:10.1016/j.bbrc.2009.03.133
2563:10.1016/j.tins.2007.01.002
1686:10.1007/s12311-021-01259-2
1222:10.1016/j.tins.2005.03.004
966:10.1016/j.tins.2007.02.005
705:The addictive property of
546:spike-timing-dependent LTD
289:voltage-gated ion channels
248:LTD occurs at synapses in
18:
3247:
3204:
3156:
3138:Auditory evoked potential
3118:
3111:
3090:
3047:
1933:The Journal of Physiology
1788:10.1007/s00018-008-8263-3
1401:. Boca Raton: CRC Press.
779:amyloid beta protein (Aβ)
609:Motor learning and memory
493:neurotransmitter receptor
374:P/Q-type calcium channels
175:heterosynaptic plasticity
27:, an economic depression.
3003:Medical Subject Headings
2605:10.1007/0-387-25443-9_18
2169:Feldman DE (July 2000).
767:Alzheimer's disease (AD)
520:Role of endocannabinoids
19:Not to be confused with
3148:Visual evoked potential
2966:10.1126/science.1213894
2915:10.1126/science.1207502
2463:10.1073/pnas.0508191102
2336:10.1073/pnas.96.17.9457
2309:Bear MF (August 1999).
889:(Short-term plasticity)
647:homosynaptic plasticity
542:nucleus accumbens (NAc)
510:acetylcholine receptors
500:LTD mechanism involves
473:prefrontal cortex (PFC)
171:homosynaptic plasticity
3232:Long-term potentiation
3184:Postsynaptic potential
3128:Bereitschaftspotential
1994:10.1038/sj.bjp.0705466
1580:10.1098/rstb.2002.1255
1562:Bear MF (April 2003).
898:Postsynaptic potential
875:Long-term potentiation
865:Homeostatic plasticity
747:ventral tegmental area
341:receptors and group I
240:
103:Long-term potentiation
78:), kainate receptors (
55:long-term potentiation
3067:Intracranial pressure
2778:Molecular Biomedicine
1425:Bear MF (July 1995).
603:signal-to-noise ratio
530:cannabinoid receptors
467:The neurotransmitter
308:AMPAR phosphorylation
238:
198:synapses between the
3237:Long-term depression
3212:Axoplasmic transport
723:medium spiny neurons
658:was released in the
200:Schaffer collaterals
165:General forms of LTD
36:long-term depression
3227:Synaptic plasticity
3219:/Nerve regeneration
2907:2011Sci...334..389H
2454:2005PNAS..10217166W
2327:1999PNAS...96.9457B
2222:. Boca Raton: CRC.
1834:(5 Pt 2): 3404–12.
1776:Cell. Mol. Life Sci
1533:. Boca Raton: CRC.
1357:1998Natur.391..892T
887:Neural Facilitation
674:facilitates LTD in
585:a back-propagating
504:and group I and II
327:medium spiny neuron
59:synaptic plasticity
16:A medical condition
3174:Membrane potential
3039:Physiology of the
2872:Connexins, a guide
2825:Nat. Rev. Neurosci
2645:Nat. Rev. Neurosci
855:Electrical synapse
749:(VTA), making the
241:
137:Neural homeostasis
21:chronic depression
3267:
3266:
3263:
3262:
3217:Neuroregeneration
3164:Neurotransmission
2881:978-1-934115-46-6
2614:978-0-387-24008-4
2379:978-0-521-59705-0
2229:978-1-4200-4414-0
1540:978-1-4200-4414-0
1408:978-0-8493-9070-8
1186:10.1159/000123040
1150:978-0-7817-6003-4
1019:978-0-87893-697-7
1008:Purves D (2008).
811:Neurodegenerative
806:Neurodegeneration
721:decreases in the
711:nucleus accumbens
514:kainate receptors
498:perirhinal cortex
489:perirhinal cortex
479:Perirhinal cortex
463:Prefrontal cortex
285:second messengers
179:action potentials
147:negative feedback
143:positive feedback
133:(PF-PC) synapse.
3297:
3179:Action potential
3157:Other short term
3120:Evoked potential
3116:
3115:
3033:
3026:
3019:
3010:
3009:
2987:
2977:
2944:
2926:
2901:(6054): 389–93.
2885:
2857:
2856:
2820:
2814:
2813:
2803:
2793:
2769:
2763:
2762:
2752:
2720:
2714:
2713:
2685:
2679:
2678:
2660:
2636:
2619:
2618:
2592:
2583:
2582:
2546:
2535:
2534:
2524:
2492:
2486:
2485:
2475:
2465:
2448:(47): 17166–71.
2433:
2427:
2426:
2390:
2384:
2383:
2365:
2359:
2358:
2348:
2338:
2306:
2291:
2290:
2280:
2248:
2242:
2241:
2215:
2209:
2208:
2190:
2166:
2160:
2159:
2149:
2132:(24): 10464–72.
2117:
2111:
2110:
2074:
2068:
2067:
2057:
2025:
2016:
2015:
2005:
1982:Br. J. Pharmacol
1973:
1967:
1966:
1956:
1924:
1918:
1917:
1907:
1875:
1862:
1861:
1851:
1819:
1808:
1807:
1773:
1764:
1758:
1757:
1747:
1715:
1709:
1708:
1698:
1688:
1664:
1658:
1657:
1639:
1611:
1602:
1601:
1591:
1574:(1432): 649–55.
1559:
1553:
1552:
1526:
1520:
1519:
1471:
1465:
1464:
1446:
1422:
1413:
1412:
1394:
1385:
1384:
1340:
1334:
1333:
1323:
1291:
1285:
1284:
1248:
1242:
1241:
1205:
1199:
1198:
1188:
1164:
1155:
1154:
1138:
1128:
1122:
1121:
1111:
1079:
1073:
1072:
1054:
1030:
1024:
1023:
1005:
986:
985:
949:
840:Brodmann area 25
828:synaptic pruning
761:Current research
587:action potential
525:Endocannabinoids
410:ocular dominance
384:, activation of
382:endocannabinoids
349:activation, and
329:synapses in the
253:Purkinje neurons
123:endocannabinoids
65:Characterisation
3305:
3304:
3300:
3299:
3298:
3296:
3295:
3294:
3290:Neurophysiology
3285:Neuroplasticity
3270:
3269:
3268:
3259:
3243:
3223:Neuroplasticity
3200:
3152:
3107:
3086:
3043:
3037:
2995:
2990:
2960:(6054): 315–6.
2882:
2865:
2863:Further reading
2860:
2837:10.1038/nrn2867
2821:
2817:
2770:
2766:
2721:
2717:
2686:
2682:
2658:10.1038/nrn2234
2637:
2622:
2615:
2593:
2586:
2551:Trends Neurosci
2547:
2538:
2493:
2489:
2434:
2430:
2391:
2387:
2380:
2366:
2362:
2307:
2294:
2263:(52): 14442–7.
2249:
2245:
2230:
2216:
2212:
2167:
2163:
2118:
2114:
2085:(5297): 213–5.
2075:
2071:
2026:
2019:
1974:
1970:
1939:(18): 4465–79.
1925:
1921:
1890:(5): 1599–609.
1876:
1865:
1820:
1811:
1782:(18): 2913–23.
1771:
1765:
1761:
1716:
1712:
1665:
1661:
1612:
1605:
1560:
1556:
1541:
1527:
1523:
1472:
1468:
1423:
1416:
1409:
1395:
1388:
1351:(6670): 892–6.
1341:
1337:
1292:
1288:
1253:Trends Neurosci
1249:
1245:
1210:Trends Neurosci
1206:
1202:
1165:
1158:
1151:
1129:
1125:
1094:(10): 3813–25.
1080:
1076:
1031:
1027:
1020:
1006:
989:
954:Trends Neurosci
950:
915:
911:
893:Neuroplasticity
836:
818:/activation of
816:phosphorylation
808:
763:
703:
611:
571:neuroplasticity
563:
534:corticostriatal
522:
481:
465:
430:endocannabinoid
402:
351:endocannabinoid
331:dorsal striatum
319:
310:
301:
261:parallel fibers
246:
226:protein kinases
192:
187:
167:
139:
67:
32:neurophysiology
28:
25:Long Depression
17:
12:
11:
5:
3303:
3293:
3292:
3287:
3282:
3265:
3264:
3261:
3260:
3258:
3257:
3255:Myelinogenesis
3251:
3249:
3245:
3244:
3242:
3241:
3240:
3239:
3234:
3220:
3214:
3208:
3206:
3202:
3201:
3199:
3198:
3197:
3196:
3191:
3181:
3176:
3171:
3166:
3160:
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3153:
3151:
3150:
3145:
3140:
3135:
3130:
3124:
3122:
3113:
3109:
3108:
3106:
3105:
3100:
3094:
3092:
3088:
3087:
3085:
3084:
3079:
3074:
3069:
3064:
3063:
3062:
3051:
3049:
3045:
3044:
3041:nervous system
3036:
3035:
3028:
3021:
3013:
3007:
3006:
2994:
2993:External links
2991:
2989:
2988:
2945:
2886:
2880:
2866:
2864:
2861:
2859:
2858:
2815:
2764:
2735:(6): 788–801.
2715:
2680:
2651:(11): 844–58.
2620:
2613:
2584:
2536:
2487:
2428:
2385:
2378:
2360:
2321:(17): 9457–8.
2292:
2243:
2228:
2210:
2161:
2112:
2069:
2040:(6): 1271–84.
2017:
1968:
1919:
1863:
1809:
1759:
1710:
1679:(6): 948–951.
1659:
1603:
1554:
1539:
1521:
1486:(5): 967–975.
1466:
1414:
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1123:
1074:
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987:
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906:
905:
900:
895:
890:
884:
878:
872:
867:
862:
857:
852:
847:
845:Hebbian theory
842:
835:
832:
807:
804:
796:motor learning
762:
759:
739:AMPA receptors
731:AMPA receptors
727:AMPA receptors
719:NMDA receptors
715:AMPA receptors
702:
699:
631:Purkinje cells
615:motor learning
610:
607:
562:
559:
554:amygdala (BLA)
521:
518:
506:mGlu receptors
502:NMDA receptors
480:
477:
464:
461:
449:norepinephrine
434:NMDA receptors
401:
398:
386:mGlu receptors
366:NMDA receptors
343:mGlu receptors
318:
315:
309:
306:
300:
299:Ca involvement
297:
257:climbing fiber
245:
242:
191:
188:
186:
183:
166:
163:
151:metaplasticity
138:
135:
127:parallel fiber
115:NMDA receptors
111:motor learning
95:Purkinje cells
66:
63:
15:
9:
6:
4:
3:
2:
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3110:
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3101:
3099:
3096:
3095:
3093:
3091:Primarily PNS
3089:
3083:
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3078:
3075:
3073:
3070:
3068:
3065:
3061:
3058:
3057:
3056:
3053:
3052:
3050:
3048:Primarily CNS
3046:
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2896:
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2883:
2877:
2873:
2868:
2867:
2854:
2850:
2846:
2842:
2838:
2834:
2831:(7): 459–73.
2830:
2826:
2819:
2811:
2807:
2802:
2797:
2792:
2787:
2783:
2779:
2775:
2768:
2760:
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2711:
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2580:
2576:
2572:
2568:
2564:
2560:
2556:
2552:
2545:
2543:
2541:
2532:
2528:
2523:
2518:
2514:
2510:
2506:
2502:
2498:
2491:
2483:
2479:
2474:
2469:
2464:
2459:
2455:
2451:
2447:
2443:
2439:
2432:
2424:
2420:
2416:
2412:
2408:
2404:
2401:(2): 377–88.
2400:
2396:
2389:
2381:
2375:
2371:
2364:
2356:
2352:
2347:
2342:
2337:
2332:
2328:
2324:
2320:
2316:
2312:
2305:
2303:
2301:
2299:
2297:
2288:
2284:
2279:
2274:
2270:
2266:
2262:
2258:
2254:
2247:
2239:
2235:
2231:
2225:
2221:
2214:
2206:
2202:
2198:
2194:
2189:
2184:
2180:
2176:
2172:
2165:
2157:
2153:
2148:
2143:
2139:
2135:
2131:
2127:
2123:
2116:
2108:
2104:
2100:
2096:
2092:
2088:
2084:
2080:
2073:
2065:
2061:
2056:
2051:
2047:
2043:
2039:
2035:
2031:
2024:
2022:
2013:
2009:
2004:
1999:
1995:
1991:
1987:
1983:
1979:
1972:
1964:
1960:
1955:
1950:
1946:
1942:
1938:
1934:
1930:
1923:
1915:
1911:
1906:
1901:
1897:
1893:
1889:
1885:
1881:
1874:
1872:
1870:
1868:
1859:
1855:
1850:
1845:
1841:
1837:
1833:
1829:
1825:
1818:
1816:
1814:
1805:
1801:
1797:
1793:
1789:
1785:
1781:
1777:
1770:
1763:
1755:
1751:
1746:
1741:
1737:
1733:
1730:(4): 445–59.
1729:
1725:
1721:
1714:
1706:
1702:
1697:
1692:
1687:
1682:
1678:
1674:
1670:
1663:
1655:
1651:
1647:
1643:
1638:
1633:
1630:(3): 443–52.
1629:
1625:
1621:
1617:
1610:
1608:
1599:
1595:
1590:
1585:
1581:
1577:
1573:
1569:
1565:
1558:
1550:
1546:
1542:
1536:
1532:
1525:
1517:
1513:
1509:
1505:
1501:
1497:
1493:
1489:
1485:
1481:
1477:
1470:
1462:
1458:
1454:
1450:
1445:
1440:
1436:
1432:
1428:
1421:
1419:
1410:
1404:
1400:
1393:
1391:
1382:
1378:
1374:
1370:
1366:
1365:10.1038/36103
1362:
1358:
1354:
1350:
1346:
1339:
1331:
1327:
1322:
1317:
1313:
1309:
1305:
1301:
1297:
1290:
1282:
1278:
1274:
1270:
1266:
1262:
1259:(4): 126–30.
1258:
1254:
1247:
1239:
1235:
1231:
1227:
1223:
1219:
1216:(5): 229–38.
1215:
1211:
1204:
1196:
1192:
1187:
1182:
1179:(4): 300–17.
1178:
1174:
1170:
1163:
1161:
1152:
1146:
1142:
1137:
1136:
1127:
1119:
1115:
1110:
1105:
1101:
1097:
1093:
1089:
1085:
1078:
1070:
1066:
1062:
1058:
1053:
1048:
1045:(1): 104–17.
1044:
1040:
1036:
1029:
1021:
1015:
1011:
1004:
1002:
1000:
998:
996:
994:
992:
983:
979:
975:
971:
967:
963:
960:(4): 176–84.
959:
955:
948:
946:
944:
942:
940:
938:
936:
934:
932:
930:
928:
926:
924:
922:
920:
918:
913:
904:
901:
899:
896:
894:
891:
888:
885:
882:
879:
876:
873:
871:
868:
866:
863:
861:
858:
856:
853:
851:
848:
846:
843:
841:
838:
837:
831:
829:
825:
821:
817:
812:
803:
801:
797:
792:
788:
785:
780:
775:
773:
768:
758:
756:
752:
748:
744:
740:
736:
732:
728:
724:
720:
716:
712:
708:
698:
696:
692:
691:dentate gyrus
686:
684:
679:
677:
673:
672:acetylcholine
669:
665:
664:medial septum
661:
657:
656:acetylcholine
654:environment,
652:
648:
644:
640:
635:
632:
627:
622:
620:
616:
606:
604:
599:
595:
592:
588:
584:
580:
576:
572:
568:
558:
557:hippocampus.
555:
551:
550:visual cortex
547:
543:
539:
538:glutamatergic
536:synapses and
535:
531:
526:
517:
515:
511:
507:
503:
499:
494:
490:
486:
476:
474:
470:
460:
458:
457:acetylcholine
452:
450:
446:
442:
441:visual cortex
437:
435:
431:
427:
423:
419:
415:
411:
407:
406:visual cortex
400:Visual cortex
397:
395:
394:basal ganglia
391:
387:
383:
379:
375:
371:
370:mGlu receptor
367:
363:
359:
354:
352:
348:
347:NMDA receptor
344:
340:
336:
332:
328:
324:
314:
305:
296:
294:
290:
286:
282:
278:
274:
270:
266:
262:
258:
254:
251:
237:
233:
231:
227:
222:
219:
215:
210:
206:
201:
197:
182:
180:
176:
172:
162:
160:
156:
152:
148:
144:
134:
132:
131:Purkinje cell
128:
124:
120:
116:
112:
108:
104:
100:
96:
93:
89:
85:
81:
77:
73:
62:
60:
56:
51:
49:
45:
41:
37:
33:
26:
22:
3236:
2957:
2953:
2898:
2894:
2871:
2828:
2824:
2818:
2781:
2777:
2767:
2732:
2728:
2718:
2693:
2689:
2683:
2648:
2644:
2596:
2557:(3): 111–8.
2554:
2550:
2507:(1): 43–50.
2504:
2500:
2490:
2445:
2441:
2431:
2398:
2394:
2388:
2369:
2363:
2318:
2314:
2260:
2256:
2246:
2219:
2213:
2181:(1): 45–56.
2178:
2174:
2164:
2129:
2125:
2115:
2082:
2078:
2072:
2037:
2033:
1988:(5): 781–9.
1985:
1981:
1971:
1936:
1932:
1922:
1887:
1883:
1831:
1827:
1779:
1775:
1762:
1727:
1723:
1713:
1676:
1672:
1662:
1627:
1623:
1618:(May 2006).
1571:
1567:
1557:
1530:
1524:
1483:
1479:
1469:
1434:
1430:
1398:
1348:
1344:
1338:
1306:(1): 32–48.
1303:
1299:
1289:
1256:
1252:
1246:
1213:
1209:
1203:
1176:
1173:Neurosignals
1172:
1134:
1126:
1091:
1087:
1077:
1042:
1038:
1028:
1010:Neuroscience
1009:
957:
953:
809:
793:
789:
776:
764:
751:dopaminergic
717:relative to
704:
687:
680:
636:
623:
612:
600:
596:
590:
582:
564:
523:
482:
466:
453:
438:
426:phosphatases
418:homosynaptic
414:white matter
403:
355:
353:activation.
320:
311:
302:
269:metabotropic
247:
223:
194:LTD affects
193:
168:
140:
121:(mGluR), or
68:
52:
39:
35:
29:
3060:Wakefulness
2696:(1): 93–7.
2126:J. Neurosci
2034:J. Neurosci
1884:J. Neurosci
1828:J. Neurosci
1616:Surmeier DJ
1300:J. Neurosci
1088:J. Neurosci
689:LTD in the
660:hippocampus
639:hippocampus
579:patch clamp
422:hippocampus
196:hippocampal
190:Hippocampus
99:hippocampus
3274:Categories
3194:Inhibitory
3189:Excitatory
1673:Cerebellum
1437:(1): 1–4.
909:References
850:BCM theory
755:withdrawal
735:withdrawal
447:(CCh) and
345:, lack of
250:cerebellar
244:Cerebellum
218:ionotropic
203:Depressed
92:cerebellar
3205:Long term
3169:Chronaxie
3103:Sensation
1500:0896-6273
1281:206027600
784:glutamate
662:from the
649:(LTD) in
469:serotonin
445:carbachol
390:glutamate
378:glutamate
2984:22021844
2941:35398480
2933:22021860
2924:10921920
2853:10348436
2845:20559335
2810:35006439
2784:(1): 2.
2759:19555648
2710:19341708
2675:38811195
2667:17948030
2571:17234277
2531:21482355
2482:16278298
2423:41182888
2355:10449713
2287:18160652
2238:21204409
2205:17650728
2197:10939330
2107:46640132
2064:17287502
2012:14504143
1963:18653660
1914:10024347
1804:16405707
1796:18712277
1754:20188650
1705:33754326
1646:16675398
1598:12740110
1549:21204408
1238:22901201
1230:15866197
1195:18635946
1118:20220016
1069:15805572
1061:18400167
982:12326129
974:17335914
834:See also
772:dementia
358:striatum
323:striatum
317:Striatum
107:receptor
88:synaptic
44:synapses
3055:Arousal
2975:4458844
2954:Science
2903:Bibcode
2895:Science
2801:8607360
2750:2702854
2579:9405957
2522:3104468
2473:1288000
2450:Bibcode
2415:7954803
2323:Bibcode
2278:6673455
2156:9852584
2147:6793365
2099:8985014
2079:Science
2055:3070399
2003:1574086
1954:2614015
1905:6782177
1858:8182481
1849:6577491
1745:2841961
1696:8674158
1654:7971651
1589:1693164
1508:1419003
1453:7619513
1381:4328177
1373:9495341
1353:Bibcode
1330:7054394
1321:6564292
1273:8658594
1109:6632240
707:cocaine
548:in the
487:in the
3280:Memory
3098:Reflex
3082:Memory
3005:(MeSH)
2982:
2972:
2939:
2931:
2921:
2878:
2851:
2843:
2808:
2798:
2757:
2747:
2729:Neuron
2708:
2673:
2665:
2611:
2577:
2569:
2529:
2519:
2501:Neuron
2480:
2470:
2421:
2413:
2376:
2353:
2343:
2285:
2275:
2236:
2226:
2203:
2195:
2175:Neuron
2154:
2144:
2105:
2097:
2062:
2052:
2010:
2000:
1961:
1951:
1912:
1902:
1856:
1846:
1802:
1794:
1752:
1742:
1724:Neuron
1703:
1693:
1652:
1644:
1624:Neuron
1596:
1586:
1547:
1537:
1516:911321
1514:
1506:
1498:
1480:Neuron
1461:721329
1459:
1451:
1431:Neuron
1405:
1379:
1371:
1345:Nature
1328:
1318:
1279:
1271:
1236:
1228:
1193:
1147:
1116:
1106:
1067:
1059:
1039:Neuron
1016:
980:
972:
883:(STDP)
800:memory
643:memory
619:memory
583:before
451:(NE).
157:. The
84:mGluRs
76:AMPARs
72:NMDARs
3248:Other
3077:Sleep
2937:S2CID
2849:S2CID
2671:S2CID
2575:S2CID
2419:S2CID
2346:33710
2201:S2CID
2103:S2CID
1800:S2CID
1772:(PDF)
1650:S2CID
1512:S2CID
1457:S2CID
1377:S2CID
1277:S2CID
1234:S2CID
1065:S2CID
978:S2CID
877:(LTP)
824:NMDAR
820:GSK3β
591:after
3133:P300
3112:Both
2980:PMID
2929:PMID
2876:ISBN
2841:PMID
2806:PMID
2755:PMID
2706:PMID
2663:PMID
2609:ISBN
2567:PMID
2527:PMID
2478:PMID
2411:PMID
2395:Cell
2374:ISBN
2351:PMID
2283:PMID
2234:PMID
2224:ISBN
2193:PMID
2152:PMID
2095:PMID
2060:PMID
2008:PMID
1959:PMID
1910:PMID
1854:PMID
1792:PMID
1750:PMID
1701:PMID
1642:PMID
1594:PMID
1545:PMID
1535:ISBN
1504:PMID
1496:ISSN
1449:PMID
1403:ISBN
1369:PMID
1326:PMID
1269:PMID
1226:PMID
1191:PMID
1145:ISBN
1114:PMID
1057:PMID
1014:ISBN
970:PMID
798:and
743:GABA
641:and
617:and
567:STDP
512:and
337:and
267:and
265:AMPA
80:KARs
2970:PMC
2962:doi
2958:334
2919:PMC
2911:doi
2899:334
2833:doi
2796:PMC
2786:doi
2745:PMC
2737:doi
2698:doi
2694:383
2653:doi
2601:doi
2559:doi
2517:PMC
2509:doi
2468:PMC
2458:doi
2446:102
2403:doi
2341:PMC
2331:doi
2273:PMC
2265:doi
2183:doi
2142:PMC
2134:doi
2087:doi
2083:275
2050:PMC
2042:doi
1998:PMC
1990:doi
1986:140
1949:PMC
1941:doi
1937:586
1900:PMC
1892:doi
1844:PMC
1836:doi
1784:doi
1740:PMC
1732:doi
1691:PMC
1681:doi
1632:doi
1584:PMC
1576:doi
1572:358
1488:doi
1439:doi
1361:doi
1349:391
1316:PMC
1308:doi
1261:doi
1218:doi
1181:doi
1141:718
1104:PMC
1096:doi
1047:doi
962:doi
695:CA1
683:LTP
676:CA1
668:CA1
651:CA1
575:LTP
485:LTP
376:in
362:CA1
293:PKC
281:IP3
277:DAG
273:PLC
209:LTP
173:or
155:LTP
101:).
61:.
48:CNS
40:LTD
30:In
3276::
2978:.
2968:.
2956:.
2952:.
2935:.
2927:.
2917:.
2909:.
2897:.
2893:.
2847:.
2839:.
2829:11
2827:.
2804:.
2794:.
2780:.
2776:.
2753:.
2743:.
2733:62
2731:.
2727:.
2704:.
2692:.
2669:.
2661:.
2647:.
2643:.
2623:^
2607:.
2587:^
2573:.
2565:.
2555:30
2553:.
2539:^
2525:.
2515:.
2505:70
2503:.
2499:.
2476:.
2466:.
2456:.
2444:.
2440:.
2417:.
2409:.
2399:79
2397:.
2349:.
2339:.
2329:.
2319:96
2317:.
2313:.
2295:^
2281:.
2271:.
2261:27
2259:.
2255:.
2232:.
2199:.
2191:.
2179:27
2177:.
2173:.
2150:.
2140:.
2130:18
2128:.
2124:.
2101:.
2093:.
2081:.
2058:.
2048:.
2038:27
2036:.
2032:.
2020:^
2006:.
1996:.
1984:.
1980:.
1957:.
1947:.
1935:.
1931:.
1908:.
1898:.
1888:19
1886:.
1882:.
1866:^
1852:.
1842:.
1832:14
1830:.
1826:.
1812:^
1798:.
1790:.
1780:65
1778:.
1774:.
1748:.
1738:.
1728:65
1726:.
1722:.
1699:.
1689:.
1677:20
1675:.
1671:.
1648:.
1640:.
1628:50
1626:.
1622:.
1606:^
1592:.
1582:.
1570:.
1566:.
1543:.
1510:.
1502:.
1494:.
1482:.
1478:.
1455:.
1447:.
1435:15
1433:.
1429:.
1417:^
1389:^
1375:.
1367:.
1359:.
1347:.
1324:.
1314:.
1302:.
1298:.
1275:.
1267:.
1257:19
1255:.
1232:.
1224:.
1214:28
1212:.
1189:.
1177:16
1175:.
1171:.
1159:^
1143:.
1112:.
1102:.
1092:30
1090:.
1086:.
1063:.
1055:.
1043:58
1041:.
1037:.
990:^
976:.
968:.
958:30
956:.
916:^
822:.
774:.
757:.
697:.
678:.
436:.
339:D2
335:D1
283:)
181:.
149::
117:,
34:,
3225:/
3032:e
3025:t
3018:v
2986:.
2964::
2943:.
2913::
2905::
2884:.
2855:.
2835::
2812:.
2788::
2782:2
2761:.
2739::
2712:.
2700::
2677:.
2655::
2649:8
2617:.
2603::
2581:.
2561::
2533:.
2511::
2484:.
2460::
2452::
2425:.
2405::
2382:.
2357:.
2333::
2325::
2289:.
2267::
2240:.
2207:.
2185::
2158:.
2136::
2109:.
2089::
2066:.
2044::
2014:.
1992::
1965:.
1943::
1916:.
1894::
1860:.
1838::
1806:.
1786::
1756:.
1734::
1707:.
1683::
1656:.
1634::
1600:.
1578::
1551:.
1518:.
1490::
1484:9
1463:.
1441::
1411:.
1383:.
1363::
1355::
1332:.
1310::
1304:2
1283:.
1263::
1240:.
1220::
1197:.
1183::
1153:.
1120:.
1098::
1071:.
1049::
1022:.
984:.
964::
129:-
38:(
Text is available under the Creative Commons Attribution-ShareAlike License. Additional terms may apply.