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

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

PROVIDER: PRJNA491729 | ENA |

REPOSITORIES: ENA

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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

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

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

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

| PRJNA612082 | ENA

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

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

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Project description:Social behavioral changes are a hallmark of several neurodevelopmental and neuropsychiatric conditions, nevertheless the underlying neural substrates of such dysfunction remain poorly understood. Building evidence points to the prefrontal cortex (PFC) as one of the key brain regions that orchestrates social behavior. We used this concept with the aim to develop a translational rat model of social-circuit dysfunction, the chronic PFC activation model (CPA). Chemogenetic designer receptor hM3Dq was used to induce chronic activation of the PFC over 10 days, and the behavioral and electrophysiological signatures of prolonged PFC hyperactivity were evaluated. To test the sensitivity of this model to pharmacological interventions on longer timescales, and validate its translational potential, the rats were treated with our novel highly selective oxytocin receptor (OXTR) agonist RO6958375, which is not activating the related vasopressin V1a receptor. CPA rats showed reduced sociability in the three-chamber sociability test, and a concomitant decrease in neuronal excitability and synaptic transmission within the PFC as measured by electrophysiological recordings in acute slice preparation. Sub-chronic treatment with a low dose of the novel OXTR agonist following CPA interferes with the emergence of PFC circuit dysfunction, abnormal social behavior and specific transcriptomic changes. These results demonstrate that sustained PFC hyperactivity modifies circuit characteristics and social behaviors in ways that can be modulated by selective OXTR activation and that this model may be used to understand the circuit recruitment of prosocial therapies in drug discovery.

2023-11-05 | GSE246666 | GEO

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