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Updated: Nov 5, 2025

Restraint to Induce Stress in Mice and Rats
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Chronic restraint stress impairs cognition via modulating HDAC2 expression.

Jie Wu1,2, Cui Liu3, Ling Zhang3

  • 1Pathology Department, Comparative Medical Center, Peking Union Medical College (PUMC) and Institute of Laboratory Animal Science, Chinese Academy of Medical Science (CAMS), Panjiayuan Nanli No. 5, Beijing, 100021, People's Republic of China.

Translational Neuroscience
|May 14, 2021
PubMed
Summary

Chronic stress impairs cognition and synaptic function in mice by altering key proteins and signaling pathways. Elevated HDAC2 in the hippocampus suggests a potential target for neurodegenerative disease therapies.

Keywords:
Alzheimer’s diseasechronic stresscognitionepigeneticshistone deacetylase-2

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Stress Research

Background:

  • Chronic stress negatively impacts cognitive functions.
  • Understanding the molecular mechanisms underlying stress-induced cognitive deficits is crucial.

Purpose of the Study:

  • To investigate the effects of chronic restraint stress on cognition in mice.
  • To elucidate the probable molecular mechanisms involved in stress-induced cognitive impairment.

Main Methods:

  • Chronic stress induced using a restraint tube in mice.
  • Behavioral tests (Morris water maze, elevated plus maze, open field, novel object recognition) assessed anxiety and learning/memory.
  • Protein levels (PSD95, GluR-1, BDNF, Arc, Egr) determined via ELISA and Western blot.
  • Histone acetylation, HDAC2, PI3K/AKT pathway, and energy metabolism analyzed.

Main Results:

  • Chronic stress impaired synaptic functions, evidenced by downregulated PSD95, GluR-1, BDNF, Arc, and Egr.
  • Reduced histone acetylation and increased HDAC2 levels observed in hippocampal neurons.
  • Inhibition of the PI3K/AKT signaling pathway and energy metabolism dysfunction occurred under chronic stress.

Conclusions:

  • Elevated hippocampal HDAC2 levels in chronic stress offer potential therapeutic targets.
  • Findings provide insights into molecular mechanisms of stress-induced cognitive deficits.
  • This research may inform drug development for neurodegenerative diseases.