Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA939348 | ENA |
REPOSITORIES: ENA
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Project description:To understand the mechanisms underlying resilience to chronic stress exposure observed in mice with disinhibited SST neurons (SSTCre:γ2f/f mice), we analyzed and compared the transcriptome profiles of the medial prefrontal cortex (mPFC) from male and female control (SSTCre) and mutant (SSTCre:γ2f/f) mice, with and without exposure to 21 days of chronic variable stress (CVS). We found that SSTCre:g2f/f male, but not female, mice are resilient to CVS-induced changes in the mPFC transcriptome. The CVS-induced transcriptome of stress-resilient male mice was characterized by fewer and distinct CVS-induced gene expression changes compared to the CVS-induced transcriptome of stress-vulnerable SSTCre controls. The transcriptome of non-stressed stress-resilient male mice showed stress-like transcriptome changes along with defects in signal transduction similar to stress exposed SSTCre stress-vulnerable controls. These features of non-stressed stress-resilient mice were normalized by chronic stress exposure, along with enhancement of mRNA translation. Stress-induced differentially expressed genes of stress-vulnerable, but not stress-resilient mice were prominently associated with risk genes of human stress-related psychiatric disorders.
2024-11-05 | GSE272496 | GEO
Project description:Major depressive disorder (MDD) is a complex condition with unclear pathophysiology. Molecular disruptions within the periphery and limbic brain regions contribute to depression symptomatology. Here, we utilized a mouse chronic stress model of MDD and performed metabolomic, lipidomic, and proteomic profiling on serum plus several brain regions (ventral hippocampus, nucleus accumbens, and prefrontal cortex) of susceptible, resilient, and unstressed control mice. Proteomic analysis identified three serum proteins reduced in susceptible animals; lipidomic analysis detected differences in lipid species between resilient and susceptible animals in serum and brain; and metabolomic analysis revealed pathway dysfunctions of purine metabolism, beta oxidation, and antioxidants, which were differentially associated with stress susceptibility vs resilience by brain region. Antidepressant treatment ameliorated MDD-like behaviors and affected key metabolites within outlined networks, most dramatically in the ventral hippocampus. This work presents a resource for chronic stressinduced, tissue-specific changes in proteins, lipids, and metabolites and illuminates how molecular dysfunctions contribute to individual differences in stress sensitivity
2021-09-08 | PXD013146 | Pride
Project description:Stressful circumstances are significant contributors to mental illnesses, such as major depressive disorder. Anhedonia, which is the loss of the ability to enjoy pleasure, including rewarding activities or social contexts, is considered a key symptom of depression. Although stress-induced depression is associated with anhedonia in humans and animals, the underlying molecular mechanisms of anhedonic responses remain poorly understood. In this study, we conducted RNA sequencing to profile the medial prefrontal cortex which was substantially associated with the CUS-induced anhedonic behavioral phenotypes. Employing chronic unpredictable stress (CUS), we determined two subpopulations based on sucrose preference, which was highly correlated with social reward: susceptible (SUS, anhedonic) vs. resilient (RES, non-anhedonic) groups. We identified Syt4 as a hub gene in a gene network unique to anhedonia by conducting a weighted gene co-expression network analysis of the RNA sequencing data from the mPFC of SUS and RES mice. We also confirmed that Syt4 overexpression in the mPFC was pro-susceptible, while the Syt4 knockdown was pro-resilient; the pro-susceptible effects of SYT4 were mediated through the reduction of brain-derived neurotrophic factor (BDNF)-tropomyosin receptor kinase B (TrkB) signaling in the mPFC. These findings suggested that SYT4-BDNF interactions in the mPFC could be a crucial regulatory mechanism of anhedonic susceptibility to chronic stress.
2024-03-06 | GSE226576 | GEO
Project description:Medial prefrontal cortex transcriptome changes in germ-free mice
| PRJNA305425 | ENA
Project description:Chronic stress increases the risk of emotional disorders by altering brain structure and function. Patients with post-traumatic stress disorder (PTSD) or depressions show activity difference between the two hemispheres in the prefrontal cortex (PFC) but molecular targets associated with this laterality remains unclear. Here, we reveal that chronic social defeats later gene-expression profile differentially between the left and right medial prefrontal cortices (mPFC) in mice.
2021-06-30 | GSE114224 | GEO
Project description:Chronic stress has become a predominant factor associated with a variety of psychiatric disorders, such as depression and anxiety, in both humans and animal models. Although multiple studies have looked at transcriptome after social defeat stress, these studies focus on bulk tissues, which could dilute important molecular signatures of social interaction activated cells.In this study, we employed the Arc-TRAP mouse model in conjunction with chronic social defeat (CSD) to selectively isolate activated nuclei (AN) populations in the ventral hippocampus (vHIP) and prefrontal cortex (PFC) brain regions of resilient and susceptible animals. We subsequently performed nuclear RNA-seq to reveal the transcriptional signatures underlying susceptible and resilient behaviors and conducted a detailed analysis on these specific populations.Our findings provide a novel view of stress-exposed neuronal activation and the molecular response mechanisms, which may have important implications for understanding the development of stress-related disorders.
2023-08-14 | GSE240573 | GEO
Project description:Here we show that ?-catenin mediates pro-resilient and anxiolytic effects in mice in the nucleus accumbens (NAc), a key brain reward region, an effect that is mediated by ?-catenin signaling in D2-type medium spiny neurons (MSNs) specifically. Conversely, blocking ?-catenin function in NAc promotes susceptibility to chronic stress, and we show evidence of robust suppression of ?-catenin transcriptional activity in the NAc both of depressed humans examined postmortem as well as of mice that display a susceptible phenotype after chronic stress, with a converse upregulation in mice that are stress resilient. Using ChIP-seq, we demonstrate a global, genome-wide enrichment of ?-catenin in the NAc of resilient mice, and specifically identify Dicer1—important in small RNA (e.g., microRNA [miRNA]) biogenesis—as a critical ?-catenin target gene involved in mediating a resilient phenotype. Small RNA-seq after excising ?-catenin from the NAc in the context of chronic stress reveals dynamic ?-catenin-dependent miRNA regulation associated with resilience. Control: 2 samples, Resilient: 2 samples, Susceptible: 2 samples; DNA input: 1 sample.
2014-11-13 | E-GEOD-61294 | biostudies-arrayexpress
Project description:To understand the consequences of chronic exposure to fluoxetine during postnatal life on global transcriptional changes withing the rat medial prefrontal cortex in adulthood. To understand the consequences of chronic exposure to fluoxetine during postnatal life on global transcriptional changes withing the rat medial prefrontal cortex in adulthood.
2024-06-30 | GSE270730 | GEO
Project description:To understand the consequences of chronic exposure to fluoxetine during juvenile life on global transcriptional changes withing the rat medial prefrontal cortex in adulthood. To understand the consequences of chronic exposure to fluoxetine during juvenile life on global transcriptional changes withing the rat medial prefrontal cortex in adulthood.
2024-06-30 | GSE270731 | GEO
Project description:Gene expression analysis of prefrontal cortex in mice exposed to chronic mild stress
| PRJNA215173 | ENA