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Investigation of Poststroke Depression Following a Nucleus Accumbens Infarct in Mice
Jonathan Bouchard1, Béatrice Daigle1, Adeline Collignon1
1Faculty of Medicine, Department of Psychiatry and Neuroscience and CERVO Brain Research Center (J.B., B.D., A.C., L.B.B., L.M.B., V.R., L.D.-A., M. Lebel, M. Lévesque, C.M.), Université Laval, Quebec, QC, Canada.
Stroke
|June 19, 2025
Summary
This study investigated if blood-brain barrier (BBB) changes in the nucleus accumbens (NAc) contribute to poststroke depression (PSD). While ET-1 induced BBB changes, it did not cause a clear PSD phenotype in mice.
Area of Science:
- Neuroscience
- Molecular Biology
- Pathophysiology
Background:
- Poststroke depression (PSD) affects approximately 33% of stroke survivors.
- Blood-brain barrier (BBB) dysfunction in the nucleus accumbens (NAc) is linked to depressive behaviors.
- Neurovascular alterations are observed in major depression.
Purpose of the Study:
- To investigate if BBB changes in the NAc contribute to PSD.
- To explore the effects of focal stroke in the NAc on BBB integrity and gene expression.
- To assess if NAc stroke induces a PSD-like phenotype in mice.
Main Methods:
- Focal stroke induced in the NAc of male mice using endothelin-1 (ET-1).
- Assessed infarct size, BBB integrity (dextran dye, MRI), and gene expression.
- Evaluated behavioral tests for depressive- and anxiety-like behaviors.
Main Results:
- ET-1 injection caused BBB hyperpermeability and gliosis in the NAc.
- BBB gene expression was altered post-stroke and by surgery.
- Limited PSD-like symptoms were observed, but surgery affected behavior.
Conclusions:
- ET-1 induced stroke in the NAc did not produce a clear PSD phenotype in male mice.
- Highlights technical challenges of deep brain lesions and the need to control for vascular alterations.
- Provides insights for developing mouse models of deep brain lesions.

