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Gene Expression data from the dentate gyrus of the defeated and control mice

ABSTRACT: Using various animal models, epigenetic mechanisms have been shown to be mediating the negative effects of chronic stressful events on the progression of depression and other neuropsychiatric disorders. However, non-coding RNAs, another layer of epigenetic regulation is relatively lesser studied in this context. We used mRNA microarrays to uncover dysregulation in miRNA-mRNA networks in the neurogenic dentate gyrus (DG) region of chronic social defeat stress (CSDS)-induced depressed mice by identifying tagets of the selected miRNAs from this list

ORGANISM(S): Mus musculus

PROVIDER: GSE132819 | GEO | 2019/07/17

REPOSITORIES: GEO

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Project description:Major depression is a multidimensional disorder highly prevalent in modern society. Although several classes of antidepressants (ADs) are currently available to treat depression, the effectiveness of treatment is still limited, as many patients do not show full remission; thus, there is a need to find better patients’ directed therapeutic strategies. Neuroplastic changes in several brain regions, namely in the hippocampal dentate gyrus (DG), are amongst the best correlates of depression and of ADs actions. In this study the targets and molecular mediators of chronic stress and of four ADs from different pharmacological classes (fluoxetine, imipramine, tianeptine and agomelatine) were investigated in the DG. Using the unpredictable chronic mild stress (uCMS) animal model of depression, the molecular commonalities and specificities of the ADs were determined. All ADs, except agomelatine, could reverse the behavioral deficits produced by uCMS, and the neuroplastic changes in the DG; agomelatine reversed only the anhedonic profile in the sucrose consumption test. Chronic stress induced mild but relevant molecular changes that were mostly reversed by fluoxetine, imipramine and tianeptine. Fluoxetine reduced pro-inflammatory response and increased cell metabolism pathways. Its actions were mostly dependent on molecular changes occurring in neurons. Similarities were found between imipramine and tianeptine molecular actions and targets, as both activated pathways related to cellular protection. Moreover, no particular neural cell type enrichment was found with both treatments. Agomelatine presented a very dissimilar molecular pattern impacting greatly on Rho-GTPases-related pathways in oligodendrocytes and neurons. The recognition of these molecular alterations contributes to the understanding of the processes implicated in the onset and treatment of depression and may pave the way for more effective therapeutic interventions. We compared gene expresssion in the dentate gyros of rats which were either untreated, exposed to unpredictable chronic mild stress, or exposed to the same stress and treated with either fluoxetine, imipramine, tianeptine, or agomelatine

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Gene Expression data from the dentate gyrus of the defeated and control mice

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