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A single-nucleus transcriptomic analysis reveals hippocampal neuronal alterations linked to anxiety- and
Kangcheng Luo1, Mengting Zhang1, Qianwen Tu1
1Department of Colorectal and Anal Surgery, Zhongnan Hospital of Wuhan University, No. 169, Donghu Road, Wuchang District, Wuhan, Hubei province, 430071, China; Quality Control Center of Colorectal and Anal Surgery, Health Commission of Hubei Province, No. 169, Donghu Road, Wuchang District, Wuhan, Hubei province, 430071, China; Wuhan Clinical Research Center for Constipation and Pelvic Floor Disorders, Zhongnan Hospital of Wuhan University, No. 169, Donghu Road, Wuchang District, Wuhan, Hubei province, 430071, China.
Abstract:
Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, is a chronic inflammatory disorder that often has extraintestinal manifestations. Anxiety and depression are common in patients with IBD. Recent studies have demonstrated that the hippocampus contributes to the pathogenesis of psychiatric comorbidities in IBD. Therefore, this study aimed to elucidate the cellular and molecular changes in the hippocampus before and after the induction of colitis through single-nucleus sequencing technology, thus providing insights into the comorbidity mechanisms. Colitis mouse models were established by adding dextran sulfate sodium (DSS) to the drinking water. Behavioral tests were used to evaluate anxiety- and depression-like behaviors. Single-nucleus RNA sequencing analysis was carried out to identify specific neuronal subpopulations in the hippocampal and their functions. We found that DSS-treated mice exhibited intestinal inflammation and anxiety- and depression-like behaviors. The number of cells in the DG cluster and the Meis2 cluster decreased significantly after DSS treatment. Further analyses revealed that the DG-2 cluster might represent a key hippocampal subpopulation mediating the association between IBD and anxiety/depression. This study provides novel insights into the role of neuronal cells in the pathology of the comorbidity. Neurons of the DG-2 subpopulation may serve as a potential target for future therapeutic interventions.
