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Extinction Training During the Reconsolidation Window Prevents Recovery of Fear
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LncRNA Dleu2 regulates fear extinction memory through Celf2-driven synaptic plasticity.

Ziwei Pi1, Jiazhi Jiang1, Lixin Dong1

  • 1Brain Research Center, Zhongnan Hospital of Wuhan University, Wuhan, China; Department of Neurosurgery, Zhongnan Hospital of Wuhan University, Wuhan, China.

Brain Research Bulletin
|February 2, 2026
PubMed
Summary

Long noncoding RNA (lncRNA) Dleu2 is crucial for fear extinction memory in the brain. Its regulation of Celf2 impacts synaptic plasticity and memory, offering a potential therapeutic target for memory disorders.

Keywords:
Celf2Dleu2Fear extinctionLearning and memorySynaptic plasticity

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Long noncoding RNAs (lncRNAs) are key regulators of brain function.
  • The role of lncRNAs in fear extinction memory is not well understood.

Purpose of the Study:

  • To investigate the role of lncRNAs in fear extinction memory.
  • To identify specific lncRNAs involved in this process and elucidate their mechanisms.

Main Methods:

  • RNA capture sequencing in the infralimbic prefrontal cortex (ILPFC).
  • Antisense oligonucleotide (ASO)-mediated knockdown of Dleu2.
  • Chromatin Interaction Analysis by Paired-End Tag sequencing (CHIRP-seq) and Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq).
  • Celf2 knockdown and assessment of dendritic spine density.

Main Results:

  • Identified Dleu2 as a processed-transcript lncRNA involved in fear extinction.
  • Dleu2 knockdown impaired extinction memory, highlighting its essential role.
  • Dleu2 binds to the intronic region of Celf2, enhancing its transcription and chromatin accessibility.
  • Celf2 knockdown in ILPFC mimicked extinction deficits and reduced dendritic spine number.

Conclusions:

  • lncRNA Dleu2 plays a critical role in fear extinction memory by regulating Celf2 expression.
  • This mechanism involves modulating chromatin accessibility and promoting Celf2 transcription, impacting synaptic plasticity.
  • Dleu2 represents a potential therapeutic target for memory-related disorders.