ArticleTranslational psychiatry2022
C1q deletion exacerbates stress-induced learned helplessness behavior and induces neuroinflammation in mice.
Article in Translational psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.
- C1q as a target molecule to treat human disease: What do mouse studies teach us?Frontiers in immunology · 2022Pooled it
- The Role of Complement and CD4 T Cells in Preeclampsia and Offspring Neurodevelopment.Current opinion in physiology · 2026Article
- [C1q-neutralizing antibodies improves postpartum depressive-like behaviors in mice by regulating the C1q/C3 pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Knowing the enemy: strategic targeting of complement to treat Alzheimer disease.Nature reviews. Neurology · 2025Review
- KCC2 inhibition and neuronal hyperexcitability promote extrinsic apoptosis dependent upon C1q.Frontiers in molecular neuroscience · 2025Article
- Serum proteomic changes related to residual impairment in remittent depression are associated with immune and inflammatory processes.Scientific reports · 2024Article
- The complement system: a potential target for the comorbidity of chronic pain and depression.The Korean journal of pain · 2024Article
- Dysregulation of complement system in neuropsychiatric disorders: A mini review.Biomarkers in neuropsychiatry · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
Increased levels of pro-inflammatory cytokines have been reported in postmortem brain samples and in the blood of depressed subjects. However, the inflammatory pathways that lead to depressive-like symptoms are not well understood. Using the learned helplessness (LH) model of depression, we examined the role of C1q, the initiator of classical complement pathway in mediating stress-induced depressive-like behavior in mice. We observed no significant changes in social behavior, despair behavior, spatial memory, and aggressive behavior between the wild type (WT) and C1q knockout (KO) mice. However, C1q deletion exacerbated the inescapable electric foot shock-induced learned helplessness behavior in mice. We found significant reductions in C1q mRNA levels in the prefrontal cortex (PFC) of WT helpless mice as compared to the naïve mice. Increased levels of pro-inflammatory cytokines were found in the PFC of C1q KO mice. These findings suggest that classical complement pathway-mediated learned helplessness behavior is accompanied by neuroinflammatory changes under stressful conditions.
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