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Related Concept Videos

Long-term Potentiation01:25

Long-term Potentiation

Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Long-term Potentiation01:35

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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Neuroplasticity

Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.
Long-term Depression01:03

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Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
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Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Neurogenesis and Regeneration of Nervous Tissue01:15

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In the CNS, neurogenesis, the birth of new neurons from stem cells, is limited to the hippocampus in adults. In other regions of the brain and spinal cord, neurogenesis is almost non-existent due to inhibitory influences from neuroglia, especially oligodendrocytes, and the absence of growth-stimulating cues. The myelin produced by oligodendrocytes in the CNS inhibits neuronal regeneration. Furthermore, astrocytes proliferate rapidly after neuronal damage, forming scar tissue that physically...

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Investigation of Synaptic Tagging/Capture and Cross-capture using Acute Hippocampal Slices from Rodents
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Neocortical synaptic proliferation following forebrain-dependent trace associative learning.

Lily S Chau1, Ashley S Davis, Roberto Galvez

  • 1Behavioral Neuroscience Division, Psychology Department, University of Illinois at Urbana-Champaign, 603 East Daniel Street, Champaign, IL 61820, USA. chau6@illinois.edu

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|February 13, 2013
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Summary

Trace associative learning, specifically whisker-trace-eyeblink conditioning, enhances synapsin I expression in the neocortex. This indicates that learning promotes synaptic proliferation and neocortical synaptic modification.

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Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Learning and Memory

Background:

  • Behavioral studies suggest learning causes neocortical synaptic changes.
  • Neocortical synaptic modifications after forebrain-dependent trace associative learning remain understudied.
  • Whisker-trace-eyeblink (WTEB) conditioning shows altered metabolic activity in the neocortex, hinting at synaptic plasticity.

Purpose of the Study:

  • To directly examine neocortical synaptic modifications following WTEB conditioning.
  • To investigate changes in synapsin I expression as a marker for synapse number.
  • To correlate metabolic changes with synaptic alterations after trace associative learning.

Main Methods:

  • Assessed synapsin I expression in the primary somatosensory neocortex of mice after WTEB conditioning.
  • Compared synapsin I levels in trace-paired-conditioned mice, unpaired-conditioned mice, and naïve mice.
  • Replicated previous findings on cytochrome oxidase expression changes in conditioned barrels.

Main Results:

  • Synapsin I expression was significantly elevated in the neocortex of trace-paired-conditioned mice compared to controls.
  • This increase in synapsin I suggests WTEB conditioning induces synaptic proliferation.
  • Cytochrome oxidase expression confirmed a learning-specific expansion in conditioned barrels, consistent with prior research.

Conclusions:

  • Whisker-trace-eyeblink conditioning leads to increased synapsin I expression, indicating synaptic proliferation in the neocortex.
  • Synaptic proliferation likely contributes to the learning-induced metabolic increases observed in conditioned barrels.
  • These findings provide direct evidence that trace associative learning drives neocortical synaptic modification.