ArticleTranslational psychiatry2025
mPFC DCC coupling with CaMKII
Article in Translational psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Exploring the shared genetic architecture and causal relationship between childhood maltreatment and psychiatric disorders.Molecular psychiatry · 2026Article
- Article
- Calpain-1 Potentiates Periodontal Regeneration via PHLPP1-ERK-Driven Osteogenesis in Periodontal Ligament Stem Cells.International dental journal · 2026Article
- Exercise Attenuates Neuroinflammation in Chronic Restraint Stress Induced Depression Model by Downregulating GDF15 Expression.Journal of immunology research · 2026Article
- How stressful life events are associated with depression: the mediating pathway of security in a clinical adolescent sample.Frontiers in psychiatry · 2026Article
- Electroacupuncture Prevents Against AD-Like Phenotypes in APP/PS1 Mice: Investigation of the Mechanisms From Cerebral Microangiopathy.CNS neuroscience & therapeutics · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
A longed lack of control over harmful stimuli can lead to learned helplessness (LH), a significant factor in depression. However, the cellular and molecular mechanisms underlying LH, and eventually behavioral despair, remain largely unknown. The deleted in colorectal cancer (dcc) gene is associated with the risk of depression. However, the therapeutic potential and regulation mechanism of DCC in behavioral despair are still uncertain. In this study, we showed that depressive stimulators, including LH, lipopolysaccharide, and unpredictable chronic mild stress, triggered an elevation in DCC expression in the medial prefrontal cortex (mPFC). Additionally, elevated DCC expression in the mPFC was crucial in inducing behavioral despair, as evidenced by the induction of behavioral despair in normal mice and exacerbation of behavioral despair in LH mice upon DCC overexpression. By contrast, neutralizing DCC activity ameliorated LH-induced behavioral despair. Importantly, we elucidated that pathological DCC expression was attributable to the excessive excitation of CaMKII
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