Gut microbiota perturbations by social defeat in Syrian hamsters
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB40499 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Behavioral analysis confirmed that the 14-day social defeat sessions resulted in induction of depressive-like states measured in social interaction and light/dark tests. The combined data show that stress-induced depressive states are associated with molecular and structural changes that demyelinate the prefrontal cortex.
2017-06-12 | GSE84572 | GEO
Project description:This study assessed the effects of social defeat stress on the murine colonic epithelial transcriptome
2022-02-18 | GSE196614 | GEO
Project description:This study aimed to investigate the effects of depression on transcriptome in ileum using a subchronic and mild social defeat stress (sCSDS) model. In addition to exhibiting social deficit and hyperphagia-like behavior, the sCSDS mice keep much more water in their body than control mice. In order to investigate the effect of social defeat stress on not only central nervous system but also function of gastrointestinal tract, the gene expression in ileum of stressed mice was compared with control mice. We used microarrays to detail the gene expression after 10 days of social defeat stress and identified distinct classes of down-regulated genes during this process. The duration of physical contacts was set at 5 min after the first attack bite at Day 1, and then was reduced 0.5 min per day from Day 2 to Day 10.
2016-08-03 | E-GEOD-64004 | biostudies-arrayexpress
Project description:We have analysed changes in the hypothalamus using iTRAQ proteomics 4 plex from mice exposed to social defeat protocol using Qexactive and Orbitrap Velos
2024-05-28 | PXD005644 | Pride
Project description:This study tested the effects of repeated social defeat (RSD) on gene expression in peripheral blood mononuclear cells (PBMC), and examined the extent to which these effects were abrogated by depletion of CD11b+ cells (monocytes). Study Type: Risk prediction Gene expression profiling was carried out on peripheral blood mononuclear cell (PBMC) mRNA samples collected from 18 mice randomized to either 6 cycles of repeated social defeat (RSD, n=9) or to home cage control (HCC, n=9) conditions. PBMC samples were pooled into 3 groups of n=3 samples in each condition, and Illumina Mouse Ref-8 BeadArray assays were performed on approximately 1 million total PBMC and 1 million PBMC from which CD11b+ cells were immunomagnetically depleted by MACS. The primary research questions are 1) whether expression of pro-inflammatory genes is altered by RSD, and 2) whether depletion of CD11b+ cells (monocytes) abrogates these effects.
2013-11-04 | E-GEOD-47154 | biostudies-arrayexpress
Project description:This study aimed to investigate the effects of depression on transcriptome in ileum using a subchronic and mild social defeat stress (sCSDS) model. In addition to exhibiting social deficit and hyperphagia-like behavior, the sCSDS mice keep much more water in their body than control mice. In order to investigate the effect of social defeat stress on not only central nervous system but also function of gastrointestinal tract, the gene expression in ileum of stressed mice was compared with control mice. We used microarrays to detail the gene expression after 10 days of social defeat stress and identified distinct classes of down-regulated genes during this process.
2016-08-03 | GSE64004 | GEO
Project description:While stressful life events are an important cause of psychopathology such as Post-Traumatic Stress Disorder (PTSD) and Major Depressive Disorder (MDD), most individuals exposed to chronic stress remain psychologically unperturbed. The molecular mechanisms such variations in stress resilience remain to be explored. Utilizing a mouse social defeat paradigm as a model for chronic social stress exposure, we segregated socially defeated c57bl/6J mice into Susceptible and Unsusceptible groups based on scores of social avoidance, and these groups differ along multiple behavioral and physiological domains. To explore neuroplastic changes within the mesolimbic dopamine circuit that may explain variations in susceptibility, we examined global patterns of gene expression within the VTA (ventral tegmental area) and the NAc (nucleus accumbens). Tissue punches of NAc and VTA were obtained from either non-defeated control, Susceptible and Unsusceptible mice approximately 48 hours after the cessation of social defeat stress. Data from Illumina sentrix gene expression microarrays revealed three main findings: (1) the total number of genes significantly up or downregulated was considerably higher within the NAc, (2) the Unsusceptible phenotype was associated with the regulation of a much higher number of genes, and (3) as compared to the NAc, the VTA displayed far fewer genes that were identically regulated in both Susceptible and Unsusceptible groups. Taken together, these data strongly suggest that the VTA is an important substrate for transcriptional changes that can be correlated with variations in Susceptibility. In addition, they suggest that changes in anxiety (found in both Susceptible and Unsusceptible groups) versus changes in reward behavior (found only in Susceptilbe mice) can be explained by gene expression changes within the mesolimbic dopamine circuit. Keywords: neural stress response
2007-09-01 | GSE8870 | GEO
Project description:We used microarrays to identify the gene with altered expression in the hippocampus of depression mouse model with repeated social defeat stress campared to control mice.
2023-02-17 | GSE218742 | GEO
Project description:sychological stress and affective disorders are clinically associated with hypertension and vascular disease, but the biological links between the conditions have not been fully explored. To examine this relationship, we used chronic social defeat (CSD) stress, which produces anxiety-like and depressive-like behavioral declines in susceptible mice. In such mice, CSD also produces cerebrovascular microbleeds in scattered locations. Here, we showed further evidence of vascular pathology and blood–brain barrier breakdown by visualizing plasma immunoglobulins and erythrocytes within the parenchyma and perivascular spaces of CSD brains. To further characterize the impact of stress on the cerebrovasculature, brain endothelial cells (bECs) were isolated, and global gene expression profiles were generated. Bioinformatic analysis of CSD-induced transcriptional changes in bECs showed enrichment in pathways that delineate the vascular response to injury. These pathways followed a temporal sequence of inflammation, oxidative stress, growth factor signaling, and wound healing (i.e., platelet aggregation, hemostasis, fibrinogen deposition, and angiogenesis). Immunohistochemical staining for markers of fibrinogen deposition and angiogenesis confirmed the existence of the markers at the sites of vascular disruptions. Recovery after CSD cessation was marked by recruitment of leukocytes perhaps participating in vascular repair. The data suggest that co-morbidity of affective disorders and vascular diseases may be attributed in part to a common link in altered endothelial cell function
2020-08-13 | GSE156123 | GEO
Project description:Stress is associated with an increased prevalence of anxiety and depression. Repeated social defeat (RSD) stress in mice increases the release of monocytes from the bone marrow that are recruited to the brain by microglia. These monocytes enhance inflammatory signaling and augment anxiety. Moreover, RSD promotes stress sensitization, in which exposure to acute stress 24 days after cessation of RSD causes anxiety recurrence. The purpose of this study was to determine whether microglia were critical to stress sensitization and exhibited altered gene expression 24 days after RSD.
2018-12-21 | GSE124169 | GEO