Gene expression analysis of brain cortex of corticosterone-treated rats
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE9797 | GEO | 2007/12/12
SECONDARY ACCESSION(S): PRJNA105119
REPOSITORIES: GEO
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Project description:Animal models represent a very useful tool for the study of depressive-like behaviour and for the evaluation of the therapeutic efficacy of antidepressants. Nevertheless, gene expression patterns of these different animal models and whether genes classically associated to human major depression are present in these genetic profiles remain unknown. Gene expression was evaluated in an animal model of depression: corticosterone-treated rats. Gene expression analyses were carried out using the Affymetrix® GeneChip® technology. Experiment Overall Design: In total, 19 animals were studied, 10 corticosterone-treated rats and 9 control rats
2008-06-16 | E-GEOD-9797 | biostudies-arrayexpress
Project description:Animal models represent a very useful tool for the study of depressive-like behaviour and for the evaluation of the therapeutic efficacy of antidepressants. Nevertheless, gene expression patterns of these different animal models and whether genes classically associated to human major depression are present in these genetic profiles remain unknown. Gene expression was evaluated in an animal model of depression: acute treatment with reserpine. Gene expression analyses were carried out using the Affymetrix® GeneChip® technology. Experiment Overall Design: In total, 12 animals were studied, six treated samples and six control samples
2008-06-16 | E-GEOD-9788 | biostudies-arrayexpress
Project description:Animal models represent a very useful tool for the study of depressive-like behaviour and for the evaluation of the therapeutic efficacy of antidepressants. Nevertheless, gene expression patterns of these different animal models and whether genes classically associated to human major depression are present in these genetic profiles remain unknown. Gene expression was evaluated in an animal model of depression: olfactory-bulbectomized rats. Gene expression analyses were carried out using the Affymetrix® GeneChip® technology. Experiment Overall Design: In total, 11 animals were studied, five bulbectomized rats and six sham-operated rats
2008-06-16 | E-GEOD-9789 | biostudies-arrayexpress
Project description:Animal models represent a very useful tool for the study of depressive-like behaviour and for the evaluation of the therapeutic efficacy of antidepressants. Nevertheless, gene expression patterns of these different animal models and whether genes classically associated to human major depression are present in these genetic profiles remain unknown. Gene expression was evaluated in an animal model of depression: acute treatment with reserpine. Gene expression analyses were carried out using the Affymetrix® GeneChip® technology. Keywords: Treatment vs control comparative genomics study
2007-12-12 | GSE9788 | GEO
Project description:Animal models represent a very useful tool for the study of depressive-like behaviour and for the evaluation of the therapeutic efficacy of antidepressants. Nevertheless, gene expression patterns of these different animal models and whether genes classically associated to human major depression are present in these genetic profiles remain unknown. Gene expression was evaluated in an animal model of depression: olfactory-bulbectomized rats. Gene expression analyses were carried out using the Affymetrix® GeneChip® technology. Keywords: Bulbectomized vs sham-operated comparative genomics study
2007-12-12 | GSE9789 | GEO
Project description:Microglia-mediated inflammation has been recognized as a key feature of major depressive disorder. Although hypercortisolemia is commonly observed in depressed patients and can be predictive of treatment response, how such chronic exposure to this stress hormone may influence microglia is incompletely characterized. Here, we exploited a standard mouse model of depressive-like behaviors induced by repeated peripheral administration of corticosterone. Microglia in the prefrontal cortex of mice were profiled by bulk RNA sequencing, which exhibited increased expression of inflammatory markers. In addition, single-cell RNA sequencing further identified distinct molecular patterns of microglial responses. Moreover, we revealed the up-regulation of Pu.1 and Irf8, the two central transcription factors governing microglia-mediated inflammation, in the prefrontal cortex and hippocampus of corticosterone-treated mice, which similarly occurred in depressed patients' microglia. These results have established the inflammatory signatures of microglia in the mouse model recapitulating hypercortisolemia-related depression, providing new insights into developing diagnostic and therapeutic strategies.
2024-10-01 | GSE274360 | GEO
Project description:Background: As a worldwide threat to mental health, depression affects about 322 million people globally. Recently, the role of gut microbiota dysbiosis on the pathogenesis of depression has received widespread attention, but the underlying mechanism remains elusive.Results: Corticosterone (CORT)-treated mice showed depressive-like behaviors, a reduction in hippocampal neurogenesis, and an altered composition of gut microbiota (GM). Fecal microbial transplantation (FMT) from CORT-treated mice transferred depressive-like phenotypes and their dominant GM, especially bifidobacterium and lactobacillus, to the recipients. Fecal metabolic profiling showed that the relative abundances of fecal ceramides were significantly increased in CORT-treated and the recipient mice. Metagenomic sequencing exposed that bifidobacterium and lactobacillus might be responsible for gut ceramides production in CORT-treated mice. We then found that treatment with ceramides via oral gavage was sufficient to recapitulate the depressive-like phenotypes in wild -type mice. Finally, RNA-sequencing data exposed that most of the differentially expressed genes (DEGs) between ceramides-treated mice and the control group were enriched in oxidative phosphorylation (OXPHOS) pathway. Conclusion: We conclude that chronic exposure to CORT leads to an altered GM composition and consequent ceramides production, thus leading to subtle mitochondrial OXPHOS dysfunction in hippocampus, which may contribute to the development of depressive disorders.
2024-04-01 | GSE229237 | GEO
Project description:Major depressive disorder (MDD) is the psychiatric disorder with the highest prevalence in the world. Pharmacological antidepressant treatment (AD), such as selective serotonin reuptake inhibitors [SSRI, i.e. fluoxetine (Flx)] is the first line of treatment for MDD. Despite its efficacy, lack of AD response occurs in numerous patients characterizing Difficult-to-treat Depression. ElectroConvulsive Therapy (ECT) is a highly effective treatment inducing rapid improvement in depressive symptoms and high remission rates of ~50–63% in patients with pharmaco-resistant depression. Nevertheless, the need to develop reliable treatment response predictors to guide personalized AD strategies and supplement clinical observation is becoming a pressing clinical objective. Here, we propose to establish a proteomic peripheral biomarkers signature of ECT response in an anxio/depressive animal model of non-response to AD. Using an emotionality score based on the analysis complementary behavioral tests of anxiety/depression (Elevated Plus Maze, Novelty Suppressed Feeding, Splash Test), we showed that a 4-week corticosterone treatment (35 μg/ml, Cort model) in C57BL/6JRj male mice induced an anxiety/depressive-like behavior. A 28-days chronic fluoxetine treatment (Flx, 18 mg/kg/day) reduced corticosterone-induced increase in emotional behavior. A 50% decrease in emotionality score threshold before and after Flx, was used to separate Flx-responding mice (Flx-R, n=18), or Flx non-responder mice (Flx-NR, n=7). Then, Flx-NR mice received 7 sessions of electroconvulsive seizure (ECS, equivalent to ECT in humans) and blood was collected before and after ECS treatment. Chronic ECS normalized the elevated emotionality observed in Flx-NR mice. Then, proteins were extracted from peripheral blood mononuclear cells (PBMCs) and isolated for proteomic analysis using a high-resolution MS Orbitrap. The proteomic analysis revealed a signature of 33 peripheral proteins associated with response to ECS (7 down- and 26 upregulated). These proteins were previously associated with mental disorders and involved in regulating pathways which participate to the depressive disorder etiology. remark for sample name : ECTR=Flx-NR-ES, C=cort/Veh, CFNR= Flx-NR
2022-11-01 | PXD037392 | Pride
Project description:Accumulating evidence demonstrates that the gut microbiota affects brain function and behavior, including depressive behavior. Antidepressants are the main drugs used for treatment of depression. We hypothesized that antidepressant treatment could modify gut microbiota which can partially mediate their antidepressant effects. Mice were chronically treated with one of five antidepressants (fluoxetine, escitalopram, venlafaxine, duloxetine or desipramine), and gut microbiota was analyzed, using 16s rRNA gene sequencing. After characterization of differences in the microbiota, chosen bacterial species were supplemented to vehicle and antidepressant-treated mice, and depressive-like behavior was assessed to determine bacterial effects. RNA-seq analysis was performed to determine effects of bacterial treatment in the brain. Antidepressants reduced richness and increased beta diversity of gut bacteria, compared to controls. At the genus level, antidepressants reduced abundances of Ruminococcus, Adlercreutzia, and an unclassified Alphaproteobacteria. To examine implications of the dysregulated bacteria, we chose one of antidepressants (duloxetine) and investigated if its antidepressive effects can be attenuated by simultaneous treatment with Ruminococcus flavefaciens or Adlercreutzia equolifaciens. Supplementation with R. flavefaciens diminished duloxetine-induced decrease in depressive-like behavior, while A. equolifaciens had no such effect. R. flavefaciens treatment induced changes in cortical gene expression, up-regulating genes involved in mitochondrial oxidative phosphorylation, while down-regulating genes involved in neuronal plasticity. Our results demonstrate that various types of antidepressants alter gut microbiota composition, and further implicate a role for R. flavefaciens in alleviating depressive-like behavior.
2019-04-05 | GSE129359 | GEO
Project description:The susceptibility to chronic social isolation (CSIS) is associated with development of major depression (MD). Recent studies relate MD with altered expression of synaptic proteins in specific brain regions, whereby some individuals exposed to the stressors are resistant to the stress. To explore the neurobiological underpinnings and identify candidate biomarkers for MD, a comparative proteomic approach was used to map hippocampal synaptic protein alterations of rats exposed to 6 weeks of CSIS, an animal model of depression. This model generates two stress-response phenotypes, reflecting CSIS-sensitive (depressive-like behaviour) and CSIS-resilience, assessed by sucrose preference test. Our aim was to characterize the synaptoproteome changes representative of potential long-term changes in protein expression underlying susceptibility or resilience to stress.
2020-11-27 | PXD019790 | Pride