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Gender specific transcription regulation in the prefrontal cortex following social defeat stress

ABSTRACT: Gender specific transcription regulation in the prefrontal cortex following social defeat stress

PROVIDER: PRJNA612082 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11292700_1.fastq.gz	Fastqsanger.gz
	SRR11292700_2.fastq.gz	Fastqsanger.gz
	SRR11292701_1.fastq.gz	Fastqsanger.gz
	SRR11292701_2.fastq.gz	Fastqsanger.gz
	SRR11292702_1.fastq.gz	Fastqsanger.gz

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Social defeat effect on mice prefrontal cortex

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

Gender specific transcription regulation in the prefrontal cortex following social defeat stress

Project description:Major depressive disorder (MDD) affects ~20% of the world population and is characterized by strong sexual dimorphism with females being 2-3 times more likely to develop this disorder. Previously, we demonstrated that a combination therapy with dihydrocaffeic acid (DHCA) and malvidin-glucoside (Mal-gluc) to synergistically target peripheral inflammation and stress-induced synaptic maladaptation in the brain was effective in alleviating chronic social defeat stress (CSDS)-induced depression-like phenotype in male mice. Here, we test the combination therapy in a female CSDS model for depression and compared sex-specific responses to stress in the periphery and the central nervous system. Similar to male mice, the combination treatment is also effective in promoting resilience against the CSDS-induced depression-like behavior in female mice. However, there are sex-specific differences in peripheral immune responses and differential gene regulation in the prefrontal cortex to chronic stress and to the treatment. These data indicate that while therapeutic approaches to combat stress-related disorders may be effective in both sexes, the mechanisms underlying these effects differ, emphasizing the need for inclusion of both sexes in preclinical studies using animal models.

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Small RNA Sequencing of mouse prefrontal cortex after chronic social defeat stress (CSDS)

Project description:Small RNA Sequencing of mouse prefrontal cortex after chronic social defeat stress (CSDS)

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iTRAQ-based proteomics suggests Ephb6 as a potential regulator of the ERK pathway in the prefrontal cortex of chronic social defeat stress model miceiTRAQ-based proteomics reveals Ephb6 as a potential regulator of the ERK pathway in the prefrontal cortex of chronic social defeat stress model mice

Project description:Purpose: Major depressive disorder (MDD) is a worldwide concern and devastating psychiatric disease. The World Health Organization claims that MDD leads to at least 11.9% of the global burden of disease. However, the underlying pathophysiology mechanisms of MDD remain largely unknown. Experimental design: Herein, we used a proteomic-based strategy to compare the prefrontal cortex (PFC) in chronic social defeat stress (CSDS) model mice with a control group. Based on pooled samples, differential proteins were identified in the PFC proteome using iTRAQ coupled with LC-MS/MS. Results: Ingenuity Pathway Analysis (IPA) was then followed to predict relevant pathways, with the ephrin receptor signaling pathway selected for further research. Additionally, as the selected key proteins of the ephrin receptor signaling pathway, ephrin type-B receptor 6 (EphB6) and the ERK pathway were validated by western blotting. Conclusion and clinical relevant: Altogether, increased understanding of the ephrin receptor signaling pathway in MDD is provided, which implicates further investigation of PFC dysfunction induced by CSDS treatment.

2018-07-05 | PXD007573 | Pride

Transcriptional profiling of astrocytes in the prefrontal cortex, hippocampus, accumbens nucleus and caudate putamen of a Aldh1l1-TRAP (JD130) mouse line after chronic social defeat stress

Project description:Psychiatric disorders, especially major depressive disorder, are prominent cause of disability worldwide, and in dire need of better diagnostic and therapeutic tools. In order to identify the cellular mechanisms underlying major depressive disorder we sought to understand the role of astrocytes, the most numerous subtype of glia, in this disease utilizing the TRAP gene expression analysis and chronic social defeat mouse model of depression. TRAP translational profiling is a method that allows investigators to genetically characterize specific cell types in complex tissues such as mouse brain. Using this technique we obtained RNA-Seq data from actively translating transcripts present in astrocytes. We generated the molecular profile of astrocytes from multiple brain regions affected by stress-induced depression, the prefrontal cortex, hippocampus, accumbens nucleus and caudate putamen of adult Aldh1l1-EGFP/Rpl10a (JD130) mice after chronic social defeat stress paradigm. The results of this study will further our understanding of depression pathophysiology and will provide possible targets for novel or supplementary therapies.

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Differential gene expression in prefrontal cortex from mice subject to social threat vs. control

Project description:Gene expression profiling was carried out on prefrontal cortex mRNA samples collected from 10 animals subject to repeated social threat (pooled into 2 groups of 5) and 10 animals subject to non-threatening control conditions (pooled into 2 groups of 5). The primary research question is whether gene expression differs in prefrontal cortex tissue from animals exposed to social threat vs non-threatening control conditions. Keywords: Risk prediction RNA from 5 mice/sample was pooled to generate 4 total samples: 2 from mice subject to repeated social threat, and 2 from control mice.

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Gene expression analysis of mouse brain regions after chronic social defeat stress (CSDS)

Project description:Chronic psychosocial stress is a risk factor for psychiatric disorders, and genetic factors interact in conferring susceptibility. The chronic social defeat stress (CSDS) mouse model allows identifying factors underlying resilience and susceptibility to chronic psychosocial stress. We used RNA-sequencing to identify genes and pathways affected by CSDS in three brain regions: medial prefrontal cortex (mPFC), ventral hippocampus (vHPC), and bed nucleus of the stria terminalis (BNST), of male mice from strains C57BL/6Crl and DBA/2Crl.

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Differential gene expression in prefrontal cortex from mice subject to social threat vs. control

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Repeated social defeat stress (R-SDS)-induced changes in gene expression profiles in the medial prefrontal cortex (mPFC)

Project description:Repeated social defeat stress (R-SDS)-induced changes in gene expression profiles in the medial prefrontal cortex (mPFC)

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A zinc finger transcription factor enables social behaviors by controlling transposable elements and immune response in prefrontal cortex

Project description:The neurobiological origins of social behaviors are incompletely understood. Here we utilized synthetic biology approaches to reprogram the function of ZFP189, a transcription factor whose expression and function in rodent prefrontal cortex was previously demonstrated to be protective against stress-induced social deficits. We created novel synthetic ZFP189 transcription factors including ZFP189VPR, which activates the transcription of target genes and therefore exerts opposite functional control from the endogenous, transcriptionally repressive ZFP189WT. Following viral delivery of these synthetic ZFP189 transcription factors to mouse prefrontal cortex, we observe that ZFP189-mediated transcriptional control promotes mature dendritic spine morphology on transduced pyramidal neurons. Interestingly, inversion of ZFP189-mediated transcription in this brain area, achieved by viral delivery of synthetic ZFP189VPR, precipitates social behavioral deficits in terms of social interaction, motivation, and the cognition necessary for the maintenance of social hierarchy, without other observable behavioral deficits. RNA sequencing of virally manipulated prefrontal cortex tissues reveals that ZFP189 transcription factors of opposing regulatory function have opposite influence on the expression of genetic transposable elements as well as genes that participate in adaptive immune functions. Collectively, this work reveals that ZFP189 function in the prefrontal cortex coordinates structural and transcriptional neuroadaptations necessary for complex social behaviors, and does so by regulating transposable element-rich regions of DNA to control the expression of immune-related genes. Given the evidence for a co-evolution of social behavior and the brain immune response, we posit that ZFP189 may have evolved to augment brain transposon-associated immune function as a way of enhancing an animal’s capacity for functioning in social groups.

2024-02-09 | GSE246064 | GEO

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