Plasticity of the Synaptic Modification Range

Rioult-Pedotti, Mengia-Seraina; Donoghue, John P.; Dunaevsky, Anna

doi:10.1152/jn.00164.2007

Cited by 123 publications

(103 citation statements)

References 49 publications

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“…The ability of a synapse to be modulated both positively and negatively by different frequencies supports the case for changes in synaptic strength as a candidate for the physiological basis of learning and memory (Bear et al, 1987;Thiels et al, 1996). In particular, this modifiable ability of the synapse supports recent suggestions that memories are dynamic rather than static in nature, they can be updated, erased or impaired by subsequent experiences and therefore, there is a need for synapses to reflect this by also having the ability to change strength, raise or lower synaptic thresholds (Abraham and Williams, 2008) and to shift the synaptic modification range (Rioult-Pedotti et al, 2007) rather than simply being unmodifiable and locked at a certain strength. Previously, we have described both short-and long-term synaptic plasticity in the CA1-perirhinal cortex projection.…”

Section: Introductionsupporting

confidence: 73%

Frequency-dependent changes in synaptic plasticity and brain-derived neurotrophic factor (BDNF) expression in the CA1 to perirhinal cortex projection

Kealy

Commins

2010

Brain Research

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The ability of a synapse to be modulated both positively and negatively may be considered as a plausible model for the formation of learning and memory. The CA1 to perirhinal cortex projection is one of the multiple hippocampal-neocortical projections considered to be crucially involved in memory consolidation. We and others have previously demonstrated the ability of this projection to undergo long-term potentiation (LTP), however it is currently unknown whether the CA1-perirhinal projection can also be modified negatively (i.e.

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Section: Introductionsupporting

confidence: 73%

Frequency-dependent changes in synaptic plasticity and brain-derived neurotrophic factor (BDNF) expression in the CA1 to perirhinal cortex projection

Kealy

Commins

2010

Brain Research

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“…After training, the ability to induce LTP is partially occluded, whereas LTD is increased (Rioult-Pedotti et al, 2000), suggesting that an LTP-like mechanism mediates learning-induced synaptic strengthening. In contrast, weeks after training is discontinued, both LTP and LTD return to pretraining levels, whereas synaptic connections remain strengthened in the trained hemisphere (Rioult-Pedotti et al, 2007).…”

Section: Introductionmentioning

confidence: 87%

Transient Spine Expansion and Learning-Induced Plasticity in Layer 1 Primary Motor Cortex

et al. 2008

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Experience-dependent regulation of synaptic strength in the horizontal connections in layer 1 of the primary motor cortex is likely to play an important role in motor learning. Dendritic spines, the primary sites of excitatory synapses in the brain, are known to change shape in response to various experimental stimuli. We used a rat motor learning model to examine connection strength via field recordings in slices and confocal imaging of labeled spines to explore changes induced solely by learning a simple motor task. We report that motor learning increases response size, while transiently occluding long-term potentiation (LTP) and increasing spine width in layer 1. This demonstrates learning-induced changes in behavior, synaptic responses, and structure in the same animal, suggesting that an LTP-like process in the motor cortex mediates the initial learning of a skilled task.

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“…In line with this assumption, capacity to induce LTP was reduced whereas long-term depression (LTD) was increased, suggesting that the learning-induced gain in synaptic strength reduced the capacity of LTP-formation (Rioult-Pedotti, Friedman, and Donoghue, 2000). Several weeks after skill acquisition, the ability to form LTP was restored while the horizontal connections of layer II/III remained strengthened (Rioult-Pedotti, Donoghue, and Dunaevsky, 2007). At the level of cortical physiology, motor learning induces an enlargement of the motor-cortical representation (motor maps) of the body-parts that became trained.…”

Section: Introductionmentioning

confidence: 76%

Temporal course of gene expression during motor memory formation in primary motor cortex of rats

Hertler

Buitrago

Luft

et al. 2016

Neurobiology of Learning and Memory

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Motor learning is associated with plastic reorganization of neural networks in primary motor cortex (M1) that depends on changes in gene expression. Here, we investigate the temporal profile of these changes during motor memory formation in response to a skilled reaching task in rats. mRNA-levels were measured 1h, 7h and 24h after the end of a training session using microarray technique. To assure learning specificity, trained animals were compared to a control group. In response to motor learning, genes are sequentially regulated with high time-point specificity and a shift from initial suppression to later activation. The majority of regulated genes can be linked to learning-related plasticity. In the gene-expression cascade following motor learning, three different steps can be defined: (1) an initial suppression of genes influencing gene transcription. (2) Expression of genes that support translation of mRNA in defined compartments. (3) Expression of genes that immediately mediates plastic changes. Gene expression peaks after 24h -this is a much slower time-course when compared to hippocampusdependent learning, where peaks of gene-expression can be observed 6-12h after training ended. AbstractMotor learning is associated with plastic reorganization of neural networks in primary motor cortex (M1) that depends on changes in gene expression. Here, we investigate the temporal profile of these changes during motor memory formation in response to a skilled reaching task in rats. mRNA-levels were measured 1h, 7h and 24h after the end of a training session using microarray technique. To assure learning specificity, trained animals were compared to a control group. In response to motor learning, genes are sequentially regulated with high time-point specificity and a shift from initial suppression to later activation. The majority of regulated genes can be linked to learning-related plasticity. In the gene-expression cascade following motor learning, three different steps can be defined: 1) an initial suppression of genes influencing gene transcription. 2) Expression of genes that support translation of mRNA in defined compartments. 3) Expression of genes that immediately mediates plastic changes. Gene expression peaks after 24 hours -this is a much slower time-course when compared to hippocampus-dependent learning, where peaks of geneexpression can be observed 6 to 12 hours after training ended.3

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Plasticity of the Synaptic Modification Range

Cited by 123 publications

References 49 publications

Frequency-dependent changes in synaptic plasticity and brain-derived neurotrophic factor (BDNF) expression in the CA1 to perirhinal cortex projection

Frequency-dependent changes in synaptic plasticity and brain-derived neurotrophic factor (BDNF) expression in the CA1 to perirhinal cortex projection

Transient Spine Expansion and Learning-Induced Plasticity in Layer 1 Primary Motor Cortex

Temporal course of gene expression during motor memory formation in primary motor cortex of rats

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