Knocking out Selenium Binding Protein 1 Induces Depressive-Like Behavior in Mice

Area of Science:

• Neuroscience
• Molecular Biology
• Biochemistry

Background:

• Selenium binding protein 1 (SELENBP1) is implicated in various neurological disorders.
• The specific role of SELENBP1 in depression and its associated mechanisms of oxidative stress and inflammation are not well understood.

Purpose of the Study:

• To investigate the expression levels of SELENBP1 in a mouse model of depression and in human patients with depression.
• To explore the impact of SELENBP1 knockout on inflammation, oxidative stress, and hippocampal neurogenesis in a depression model.

Main Methods:

• Analysis of SELENBP1 expression in the hippocampus of a mouse depression model and serum of human patients using the Gene Expression Omnibus database.
• Validation using blood samples from human patients and chronic unpredictable mild stress (CUMS)-induced mouse models.
• Assessment of SELENBP1 knockout effects on depressive behavior, inflammatory cytokines, oxidative stress markers, and neurogenesis (doublecortin and Ki67 staining).

Main Results:

• SELENBP1 expression was found to be decreased in the blood of human patients and the hippocampus of mice with depression.
• SELENBP1 knockout exacerbated CUMS-induced depressive behavior in mice.
• SELENBP1 deficiency led to dysregulation of inflammatory cytokines and oxidative stress, and reduced hippocampal neurogenesis.

Conclusions:

• SELENBP1 plays a role in regulating neurogenesis in depression.
• Decreased SELENBP1 levels may contribute to the pathophysiology of depression.
• SELENBP1 represents a potential biomarker for depression diagnosis and a therapeutic target for treatment.