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Restraint to Induce Stress in Mice and Rats
Published on: December 6, 2024
Decrease in doublecortin expression without neuronal cell death in rat retrosplenial cortex after stress exposure.
Nobuo Kutsuna1, Takeshi Suma, Yoshiyuki Takada
1Division of Neurosurgery, Department of Neurological Surgery, Nihon University School of Medicine, Tokyo, Japan.
Neuroreport
|December 27, 2011
Summary
Acute stress from forced swimming reduces doublecortin (DCX) expressing cells in the rat retrosplenial cortex. This decrease in neuronal plasticity markers may impair spatial learning and memory without causing cell death.
Area of Science:
- Neuroscience
- Cell Biology
- Animal Behavior
Background:
- Acute stress negatively impacts cognitive functions, particularly spatial learning and memory.
- The retrosplenial cortex is crucial for spatial memory processing.
- Doublecortin (DCX) is a marker for immature neurons involved in adult brain plasticity.
Purpose of the Study:
- To investigate the effect of acute stress on DCX expression in the rat retrosplenial cortex.
- To determine if stress alters neurogenesis or cell death in this brain region.
Main Methods:
- Rats were exposed to acute stress (forced swim) or served as controls.
- Immunohistochemistry was used to detect DCX and other neuronal markers.
- 5-bromo-2'-deoxyuridine and Fluoro-Jade B were used to assess cell proliferation and death.
Main Results:
- Stressed rats exhibited significantly fewer DCX-expressing cells in the retrosplenial cortex compared to controls.
- The proportion of DCX cells co-expressing neuronal markers remained unchanged.
- No significant changes in cell proliferation or death were observed in the retrosplenial cortex.
Conclusions:
- Acute stress markedly reduces DCX expression in the retrosplenial cortex, suggesting decreased neuronal plasticity.
- This reduction in plasticity may underlie the observed impairment in spatial learning and memory.
- Neuronal differentiation pathways appear unaffected by acute stress in this context.

