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Remote Memory and Cortical Synaptic Plasticity Require Neuronal CCCTC-Binding Factor (CTCF).

Somi Kim1, Nam-Kyung Yu1, Kyu-Won Shim2

  • 1Department of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul 08826, South Korea.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|May 2, 2018
PubMed
Summary
This summary is machine-generated.

CCCTC-binding factor (CTCF) is crucial for maintaining remote memories stored in the cortex. CTCF loss impairs long-term memory recall by affecting gene expression and synaptic plasticity in neurons.

Keywords:
3D genome architectureCTCFcortical plasticityremote memorysystems consolidation

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Epigenetics

Background:

  • Long-term memory mechanisms, particularly for remote memories stored in the cortex, remain poorly understood at the molecular level.
  • The role of 3D chromatin architecture and its regulators in neuronal plasticity and systems consolidation for long-term memory is largely unknown.
  • CCCTC-binding factor (CTCF) is a known genome architecture molecule implicated in gene regulation.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying remote memory storage in the cortex.
  • To determine the role of CTCF in neuronal plasticity and gene regulation related to long-term memory.
  • To elucidate the contribution of CTCF to systems consolidation of memory.

Main Methods:

  • Utilized conditional knockout mouse models (male and female) lacking CTCF in excitatory and inhibitory neurons.
  • Assessed memory recall using contextual fear conditioning and spatial water maze tasks.
  • Investigated synaptic plasticity via long-term potentiation (LTP) in hippocampal and cortical slices.
  • Performed RNA sequencing on cortical neurons with CTCF knockdown to analyze gene expression changes.

Main Results:

  • Conditional knockout mice lacking CTCF in excitatory neurons exhibited normal recent memory but significant impairments in remote memory recall.
  • CTCF deletion in female mice disrupted cortical LTP but not hippocampal LTP, indicating a role in cortical plasticity.
  • CTCF knockdown in cortical neurons altered the expression of genes involved in cell adhesion, synaptic plasticity, and memory.
  • Deletion in inhibitory neurons partially impaired remote memory, suggesting a broader role for CTCF.

Conclusions:

  • CTCF-mediated gene regulation in neurons is essential for the storage of remote memories in the cortex.
  • Recent memory formation in the hippocampus does not appear to be dependent on CTCF.
  • CTCF plays a critical role in regulating genes vital for learning and memory processes, contributing to systems consolidation.