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The pathogenesis of depression: Roles of connexin 43-based gap junctions and inflammation
Hong Jiang1, Meng Zhang1, Xin-Mu Li1
1State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica & Neuroscience Center, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, 100050, China.
European Journal of Pharmacology
|January 11, 2025
Summary
Connexin 43 (Cx43) blockade in the prefrontal cortex and peripheral inflammation worsen depression. These factors are interconnected, amplifying depressive behaviors and inflammatory responses in the brain.
Area of Science:
- Neuroscience
- Psychiatry
- Molecular Biology
Background:
- Depression is a global mental illness linked to inflammation.
- Connexin 43 (Cx43) is implicated in depression pathogenesis.
- Inflammation is observed in mood disorders and can exacerbate symptoms.
Purpose of the Study:
- To investigate the relationship between Cx43 and peripheral inflammation in depression.
- To understand the upstream and downstream effects of Cx43 abnormalities and inflammation.
Main Methods:
- Mice were treated with Gap27 (Cx43 mimetic peptide) in the prefrontal cortex (PFC).
- Cx43 was conditionally knocked out in the PFC.
- Mice received lipopolysaccharide (LPS) injections to induce peripheral inflammation.
Main Results:
- Cx43 blockade and LPS induced depressive-like behaviors in mice.
- Cx43 blockade altered peripheral inflammatory cytokine levels (IL-1β, IL-6, TNF-α, etc.).
- LPS-induced inflammation reduced Cx43 expression and gap junction permeability in the PFC.
Conclusions:
- Cx43 blockade in the PFC and peripheral inflammation are interconnected in depression.
- These factors mutually reinforce each other during depression induction.
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