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Related Experiment Video

Updated: May 25, 2026

Trace Fear Conditioning in Mice
07:02

Trace Fear Conditioning in Mice

Published on: March 20, 2014

Rapid synaptic potentiation within the anterior cingulate cortex mediates trace fear learning.

Giannina Descalzi1, Xiang-Yao Li, Tao Chen

  • 1Department of Physiology, Faculty of Medicine, University of Toronto, 1 King's College Circle, Toronto, Ontario M5S 1A8, Canada.

Molecular Brain
|February 7, 2012
PubMed
Summary

Trace fear learning rapidly upregulates AMPA receptors in the anterior cingulate cortex (ACC). This process requires GluN2B subunits and calcium-permeable AMPA receptors (CP-AMPARs) for memory consolidation.

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Last Updated: May 25, 2026

Trace Fear Conditioning in Mice
07:02

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Published on: March 20, 2014

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11:13

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09:49

Combined Optogenetic and Freeze-fracture Replica Immunolabeling to Examine Input-specific Arrangement of Glutamate Receptors in the Mouse Amygdala

Published on: April 15, 2016

Area of Science:

  • Neuroscience
  • Memory Research
  • Synaptic Plasticity

Background:

  • The cortex's role in long-term memory is well-studied, but its immediate contribution to fear memory formation is less understood.
  • AMPA receptor plasticity, particularly calcium-permeable AMPA receptors (CP-AMPARs), is crucial for synaptic strengthening and memory.
  • Trace fear learning involves the anterior cingulate cortex (ACC), but the specific plasticity mechanisms and the role of GluN2B subunits remain unclear.

Purpose of the Study:

  • To investigate immediate cortical contributions to trace fear memory formation.
  • To determine if plastic events occur in the ACC during trace fear learning.
  • To ascertain the requirement of GluN2B subunits in ACC plasticity and fear memory.

Main Methods:

  • Trace fear conditioning in rodents.
  • Measurement of AMPA receptor GluA1 subunit upregulation in the ACC.
  • Inhibition of NMDA receptor GluN2B subunits during training.
  • Intra-ACC injections of CP-AMPAR antagonist (NASPM).
  • Whole-cell patch clamp recordings in ACC neurons.

Main Results:

  • The ACC is essential for trace fear learning.
  • A rapid 20% upregulation of membrane AMPA receptor GluA1 subunits was observed in the ACC immediately after conditioning.
  • Inhibiting GluN2B subunits during training prevented this upregulation and disrupted memory retrieval.
  • NASPM administration post-conditioning blocked fear memory retrieval.
  • Recently activated ACC neurons showed increased NASPM sensitivity, reversible by extinction.

Conclusions:

  • Trace fear learning involves rapid GluN2B-dependent trafficking of CP-AMPARs in the ACC.
  • CP-AMPAR activity in the ACC immediately after conditioning is vital for subsequent memory consolidation.
  • This study provides in vivo evidence for immediate cortical mechanisms in fear memory formation.