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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.
Hebbian LTP
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Investigation of Synaptic Tagging/Capture and Cross-capture using Acute Hippocampal Slices from Rodents
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PirB regulates a structural substrate for cortical plasticity.

Maja Djurisic1, George S Vidal, Miriam Mann

  • 1Bio-X, James H. Clark Center, Stanford University, Stanford, CA 94305.

Proceedings of the National Academy of Sciences of the United States of America
|December 5, 2013
PubMed
Summary
This summary is machine-generated.

The paired immunoglobulin-like receptor B (PirB) protein limits learning and memory by controlling brain circuit plasticity. Removing PirB enhances synaptic plasticity and learning throughout life.

Keywords:
LTDLTPadult plasticitycircuit connectivityvisual cortex

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Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Learning and Memory

Background:

  • Experience-driven changes in neural circuits are fundamental to learning and memory.
  • Monocular deprivation (MD) is a model for studying ocular dominance (OD) plasticity, which involves changes in synaptic strength and dendritic spine density on L5 pyramidal neurons.

Purpose of the Study:

  • To investigate the role of paired immunoglobulin-like receptor B (PirB) in regulating dendritic spine density and OD plasticity in adult mice.
  • To determine how PirB deficiency affects synaptic function and the capacity for learning.

Main Methods:

  • Utilized PirB knockout (PirB-/-) and wild-type (WT) mice.
  • Assessed dendritic spine density and stability.
  • Measured synaptic plasticity, including long-term potentiation (LTP) and long-term depression (LTD).
  • Examined OD plasticity following monocular deprivation.

Main Results:

  • PirB-/- mice exhibited significantly higher dendritic spine density and stability compared to WT mice.
  • PirB deficiency was associated with increased miniature synaptic current frequency, enhanced LTP, and impaired LTD.
  • Monocular deprivation induced an increase in spine density in WT mice, but this effect was occluded in PirB-/- mice.
  • Adult PirB-/- mice showed larger and faster OD plasticity than WT mice, correlating with maintained high spine density.

Conclusions:

  • PirB acts as a negative regulator of dendritic spine and excitatory synapse density.
  • PirB influences the threshold for adult ocular dominance plasticity and learning.
  • Inhibition of PirB function enhances synaptic plasticity and learning capacity throughout life.