Gene expression analysis of brain cortex of reserpine-treated rats
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE9788 | GEO | 2007/12/12
SECONDARY ACCESSION(S): PRJNA105115
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: 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: corticosterone-treated rats. Gene expression analyses were carried out using the Affymetrix® GeneChip® technology. Keywords: Treatment vs control comparative genomics study
2007-12-12 | GSE9797 | 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. 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: 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: 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: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
Project description:To identify gene expression changes associated with Crtc1 deficiency, we performed genome-wide transcriptome profile analyses by using mouse cDNA microarrays in the cortex of Crtc1â/â and WT female mice BACKGROUND: Recent studies involve the arginine-decarboxylation product agmatine in mood regulation. Agmatine has antidepressant properties in rodent models of depression, and agmatinase (Agmat), the agmatine-degrading enzyme, is upregulated in the brain of mood disorders patients. We showed that mice lacking CREB-regulated transcription coactivator 1 (CRTC1) associate neurobehavioral and molecular depressive-like endophenotypes, as well as blunted responses to classical antidepressants. METHODS: The molecular basis of the behavioral phenotype of Crtc1â/â mice was further examined using microarray analysis. We characterized Agmat expression in the prefrontal cortex (PFC) and hippocampus (HIP) by quantitative polymerase chain reaction (qPCR), Western blot (WB) analysis, and confocal immunofluorescence microscopy. The antidepressant effect of agmatine was assessed by the forced swim test (FST). Brain-derived neurotrophic factor (BDNF) levels and eukaryotic elongation factor 2 (eEF2) phosphorylation were measured by WB. RESULTS: Microarray, qPCR and WB analyses revealed an upregulation of Agmat in Crtc1â/â PFC and HIP, where immunofluorescence microscopy showed more Agmat-expressing cells, notably parvalbumin- and somatostatin-interneurons. Acute agmatine treatment efficiently improved depressive-like behavior of Crtc1â/â mice in the FST, suggesting that exogenous agmatine has a rapid antidepressant effect through the compensation of agmatine deficit induced by upregulated Agmat. In WT mice, agmatine rapidly increased BDNF levels and eEF2 dephosphorylation, indicating that it might be a fastâacting antidepressant with NMDA receptor antagonist properties. CONCLUSIONS: Collectively, these findings support the involvement of the agmatinergic system in the depressive-like phenotype of Crtc1â/â mice, and allow a better understanding of the agmatinergic system and its putative role in major depression. RNA from cortex of 5 WT and 5 KO mice was used
2016-07-18 | E-GEOD-80633 | biostudies-arrayexpress
Project description:Background: Antidepressants (ADs) are the most common treatment for major depressive disorder (MDD). However, only about 30% of patients experience adequate response after a single AD trial, and this variability remains poorly understood. Here, we investigated microRNAs (miRNAs) as biomarkers of AD response using small RNA-sequencing in paired samples from MDD patients enrolled in a large, randomized placebo-controlled trial of duloxetine collected before and eight weeks after treatment. Results: Our results revealed differential expression of miR-146a-5p, miR-146b-5p, miR-425-3p and miR-24-3p according to treatment response. These results were replicated in two independent clinical trials of MDD, a well-characterized animal model of depression, and post-mortem human brains. Furthermore, using a combination of bioinformatics, mRNA studies and functional in vitro experiments, we showed significant dysregulation of genes involved in MAPK/Wnt signaling pathways. Conclusions: Together, our results indicate that these miRNAs are consistent markers of treatment response and regulators of the MAPK/Wnt systems.
2017-03-30 | GSE97154 | GEO
Project description:Major depressive disorder is one of the most common mental health conditions. Meningeal lymphatics are essential for drainage of molecules in the cerebrospinal fluid to the peripheral immune system. Their potential role in depression-like behaviour has not been investigated. Here, we show in mice, sub-chronic variable stress as a model of depression-like behaviour impairs meningeal lymphatics in females but not in males. Manipulations of meningeal lymphatics regulate the sex difference in the susceptibility to stress-induced depression- and anxiety-like behaviors in mice, as well as alterations of the medial prefrontal cortex and the ventral tegmental area, brain regions critical for emotional regulation. Together, our findings suggest meningeal lymphatic impairment contributes to susceptibility to stress in mice, and that restoration of the meningeal lymphatics might have potential for modulation of depression-like behaviour.
2022-07-05 | GSE201368 | GEO