期刊
PHYSIOLOGY & BEHAVIOR
卷 228, 期 -, 页码 -出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.physbeh.2020.113197
关键词
Depression; Notch2; NF-kappa B; Chronic social defeat stress; Wistar Kyoto rat
资金
- National Natural Science Foundation of China [81871068, 81671352, 91232709]
- Joint Fund for Science and Technology Innovation of Fujian [2018Y9057]
- Startup Fund for Scientific Research of Fujian Medical University [2019QH2014]
This study investigated the role of disrupted Notch signaling in chronic social defeat stress mice and depression WKY rats, identifying changes associated with depression and suggesting that increased Notch2/NF-kappa B signaling in the medial prefrontal cortex may mediate depression susceptibility.
The susceptibility to depression has been attributed to the chronic stress and genetic factors but still fails to identify definite biomarkers. The present study aimed to investigate the role of disrupted Notch signaling in the medial prefrontal cortex of the chronic social defeat stress (CSDS) mice and Wistar Kyoto (WKY) rats. RNA-sequencing and quantitative real-time PCR analyses evidenced the involvement of Notch signaling pathway in depression. Western blotting reported an increased level of Notch2 and NF-kappa B and a decreased level of Hes1 and Bcl2/Bax ratio both in the susceptible mice when compared with the control or resilient ones and in the depression WKY rats when compared with the Wistar or non-depression WKY groups. Further analysis showed that the above-mentioned changes were significantly correlated with the depression-like behaviors and that the elicited Notch2 strongly correlated with the upregulated NF-kappa B, not with the downregulated Hes1 or Bcl2/Bax ratio. In conclusion, the increased Notch2/NF-kappa B signaling in the medial prefrontal cortex may mediate depression susceptibility, providing a potential diagnostic biomarker or therapeutic target for treating major depressive disorder.
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