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Updated: Aug 8, 2026
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Trace Fear Conditioning in Mice
Published on: March 21, 2014
Fear memory retrieval induces CREB phosphorylation and Fos expression within the amygdala
J Hall1, K L Thomas, B J Everitt
1Department of Experimental Psychology, University of Cambridge, Downing Street, Cambridge, CB2 3EB. UK.
The European Journal of Neuroscience
|April 12, 2001
Summary
Retrieving fear memories activates CREB (cAMP response element-binding protein) in the amygdala, suggesting its role in memory reconsolidation. This molecular process is specific to the amygdala, not the hippocampus.
Area of Science:
- Neuroscience
- Molecular Biology
- Behavioral Science
Background:
- Fear memory retrieval can trigger protein-synthesis dependent reconsolidation within the amygdala.
- The transcription factor CREB is implicated in the formation of long-term fear memories.
Purpose of the Study:
- To investigate the molecular mechanisms underlying fear memory reconsolidation in the rat amygdala.
- To examine the role of CREB activation during fear memory retrieval.
Main Methods:
- Immunocytochemistry was used to detect phosphorylated CREB and Fos expression.
- Fear memory retrieval was induced by cue association in rats.
- Brain tissue from the amygdala and hippocampus was analyzed.
Main Results:
- Fear memory retrieval increased CREB phosphorylation in the basal, lateral, and central amygdala nuclei.
- Expression of the immediate-early gene c-fos was upregulated in the basal amygdala post-retrieval.
- No changes in phosphorylated CREB or Fos were observed in the hippocampus.
Conclusions:
- CREB activation (phosphorylation) accompanies fear memory retrieval in the amygdala.
- These findings suggest a role for CREB phosphorylation in the reconsolidation of fear memories.
- The observed molecular changes are specific to the amygdala, highlighting its central role in fear memory processing.
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