Ontology highlight
ABSTRACT:
PROVIDER: PRJNA734369 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14722500_1.fastq.gz | Fastqsanger.gz | |||
| SRR14722500_2.fastq.gz | Fastqsanger.gz | |||
| SRR14722501_1.fastq.gz | Fastqsanger.gz | |||
| SRR14722501_2.fastq.gz | Fastqsanger.gz | |||
| SRR14722502_1.fastq.gz | Fastqsanger.gz |
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Project description:We performed high-throughput profiling of gene expression in rat hippocampus in response to chronic unpredictable mild stress (CUMS) and albiflorin treatment. Total 415 differentially expressed genes (DEGs) were identified in rat hippocampus in response to albiflorin treatment compared with CUMS rats treated with saline (CUMS-Sal). We conducted the integrated metabolomics and transcriptomics analysis and found the correction of 16 biochemical pathways by albiflorin such as sphingolipids, phospholipids, tryptophan metabolism, fatty acid oxidation, and purine and pyrimidine metabolism. Our study provided deep insights into the understanding of the molecular mechanisms underlying the rapid antidepressant actions of albiflorin.
2018-01-20 | GSE109445 | GEO
Project description:Major depressive disorder is a common mood disorder. Chronic stressful life is presumably main etiology that leads to the neuron and synapse atrophies in the limbic system. However, the intermediate molecules from stress to neural atrophy remain elusive. Mice were treated by chronic unpredictable mild stress (CUMS) until demonstrating depression-like behaviors confirmed by the tests of sucrose preference, forced swimming and Y-maze. The sequencings of microRNA and mRNA from the medial prefrontal cortices were performed in CUMS-induced depression mice versus control mice to assess the molecular profiles of major depressive disorder. In the medial prefrontal cortices of depression-like mice, the levels of mRNAs that translated the proteins for the GABAergic synapses, dopaminergic synapses, myelination, synaptic vesicle cycle and neuronal growth were downregulated. miRNAs of regulating these mRNAs are upregulated. The deterioration of GABAergic and dopaminergic synapses as well as axonal growth is associated to CUMS-induced depression.
2017-02-09 | GSE81588 | GEO
Project description:In this study, depressive-like mice induced by chronic unpredictable mild stimulation (CUMS) were used to investigate the impact of psychological stress on reproduction and alterations in sperm sncRNAs. The results showed that CUMS treatments for 4 weeks induced depressive behavior in male mice and significantly affected sperm quality. The results obtained from small RNA sequencing indicated that alterations occurred in the distribution and composition of small non-coding RNAs (sncRNAs), encompassing PIWI-interacting RNAs (piRNAs), rRNA-derived small RNAs (rsRNA), and tRNA-derived small RNAs (tsRNA). Furthermore, the offspring of male mice with depressive-like behavior have a significant reduction in survival rate at 21 days after birth, and those that did survive displayed an increased susceptibility to depression.
2024-07-31 | GSE242253 | GEO
Project description:Major depressive disorder is a common mood disorder. Chronic stressful life is presumably main etiology that leads to the neuron and synapse atrophies in the limbic system. However, the intermediate molecules from stress to neural atrophy remain elusive. Mice were treated by chronic unpredictable mild stress (CUMS) until demonstrating depression-like behaviors confirmed by the tests of sucrose preference, forced swimming and Y-maze. The sequencings of microRNA and mRNA from the medial prefrontal cortices were performed in CUMS-induced depression mice versus control mice to assess the molecular profiles of major depressive disorder. In the medial prefrontal cortices of depression-like mice, the levels of mRNAs that translated the proteins for the GABAergic synapses, dopaminergic synapses, myelination, synaptic vesicle cycle and neuronal growth were downregulated. miRNAs of regulating these mRNAs are upregulated. The deterioration of GABAergic and dopaminergic synapses as well as axonal growth is associated to CUMS-induced depression.
2017-02-09 | GSE81587 | GEO
Project description:It remains unclear why many patients with depression do not respond to antidepressant treatment. In three cohorts of individuals with depression and treated with serotonin-norepinephrine reuptake inhibitor (N=424) we show that responders, but not non-responders, display an increase of GPR56 mRNA in the blood. In a small group of subjects we also show that GPR56 is also downregulated in the PFC of individuals with depression that died by suicide. In mice, we show that chronic stress induced Gpr56 downregulation in the blood and prefrontal cortex (PFC), which is accompanied by depression-like behaviour, and can be reversed by antidepressant treatment. Gpr56 knockdown in mouse PFC was is associated with depressive-like behaviors, executive dysfunction and poor response to antidepressant treatment. GPR56 peptide agonists had antidepressant-like effects and up-regulated AKT/GSK3/EIF4 pathways. Our findings uncover a potential role of GPR56 in antidepressant response.
2020-03-31 | GSE146446 | GEO
Project description:Background: Examining transcriptional regulation by existing antidepressants in key neural circuits implicated in depression, and understanding the relationship to transcriptional mechanisms of susceptibility and natural resilience, may help in the search for new therapeutics. Further, given the heterogeneity of treatment response in human populations, examining both treatment response and non-response is critical. Methods: We compared the effects of a conventional monoamine-based tricyclic antidepressant, imipramine (14 daily injections), and a rapidly acting, experimental, non-monoamine-based antidepressant, ketamine (single injection), in mice subjected to chronic social defeat stress, a validated model of depression, and used RNA-sequencing to analyze transcriptional profiles associated with susceptibility, resilience and antidepressant response and non-response in prefrontal cortex (PFC), nucleus accumbens, hippocampus, and amygdala. Results: We identified approximately equal numbers of responder and non-responder mice following ketamine or imipramine treatment. Ketamine induced more expression changes in hippocampus than other brain regions; imipramine induced more expression changes in nucleus accumbens and amygdala. Transcriptional profiles in ketamine and imipramine responders were most similar in PFC, where the least transcriptional regulation occurred for each drug. Non-response reflected both the lack of response-associated gene expression changes and unique gene regulation. In responders, both drugs reversed susceptible associated transcriptional changes as well as induced resilient associated transcription in PFC, with effects varying by drug and brain region studied. Conclusions: We generated a uniquely large resource of gene expression data in four inter-connected limbic brain regions implicated in depression and its treatment with imipramine or ketamine. Our analyses highlight the PFC as a key site of common transcriptional regulation by both antidepressant drugs and in both reversing susceptibility and inducing resilience associated molecular adaptations. In addition, we found region-specific effects of each drug suggesting both common and unique effects of imipramine versus ketamine. mRNA profiles of susceptibility to chronic social defeat stress as well as treatment response were generated across 4 separate brain regions, with a sample size of 3-5 per group.
2016-07-27 | E-GEOD-81672 | biostudies-arrayexpress
Project description:Major depressive disorder (MDD) has caused a heavy burden on society and affected over 350 million patients worldwide currently. However, there have been 30-50% MDD patients with non-response to antidepressants. Chronic unpredictable mild stress (CUMS) has been considered as a critical trigger factor for MDD, the pathological mechanism of which is strongly associated with stimulating inflammatory responses. Xiaoyaosan (XYS), as a classic famous prescription, has been proven effective for alleviating CUMS induced injury. Purpose: This study aimed to clarify the potential anti-inflammatory mechanisms of XYS treating CUMS model mice. Study design and methods: The therapeutic effects of XYS on the behavior and inflammatory indicators of CUMS model mice were determined. Ultra high performance liquid chromatography - High resolution mass spectrometry (UPLC-HRMS) was applied identify the compounds of XYS and proteomics analysis was utilized to explore the potential mechanism. Additionally, molecular docking and further in vivo experiments were conducted to verify the results of proteomics analysis. Results: The in vivo experiments confirmed XYS not only could significantly improve sucrose preference percentage and behavioral indicators of open field test, but also could decrease the serum levels of inflammatory indexes (CORT, hs-CRP, NFκB, FIB and Lp-PLA2) and inhibit the protein expressions of IL-6 and TNF-α in brain of CUMS model mice. Proteomics analysis presented that MAPK signaling pathway might be the important anti-inflammatory mechanism of XYS alleviating CUMS induced injury. UPLC-HRMS identify the compounds of XYS, which were taken into molecular docking to analysis the interaction between XYS and MYDGF, PKC, MAP4K4, P-p65, p65, P-IKBα, and IKBα. It was validated that XYS could exert regulatory effects on the MYDGF/MAP4K4/NF-κB signaling pathway in CUMS model mice. Conclusion: In conclusion, this study first demonstrated that XYS could alleviate inflammation in CUMS model mice via modulating MYDGF/MAP4K4/NF-κB signaling pathway.
2024-06-25 | PXD053391 |
Project description:Selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine are the most common treatment for major depression. However, approximately 50% of depressed patients fail to achieve an effective treatment response. Understanding how gene expression systems relate to treatment responses may be critical for understanding antidepressant resistance. Transcriptome profiling allows for the simultaneous measurement of expression levels for thousands of genes and the opportunity to utilize this information to determine mechanisms underlying antidepressant treatment responses. However, the best way to relate this immense amount of information to treatment resistance remains unclear. We take a novel approach to this question by examining dentate gyrus transcriptomes from the perspective of a stereotyped fluoxetine-induced gene expression program. Expression programs usually represent stereotyped changes in expression levels that occur as cells transition phenotypes. Fluoxetine will shift transcriptomes so they lie somewhere between a baseline state and a full-response at the end of the program. The position along this fluoxetine-induced gene expression program (program status) was measured using principal components analysis (PCA). The same expression program was initiated in treatment-responsive and resistant mice but treatment response was associated with further progression along the fluoxetine-induced gene expression program. The study of treatment-related differences in gene expression program status represents a novel way to conceptualize differences in treatment responses at a transcriptome level. Understanding how antidepressant-induced gene expression program progression is modulated represents an important area for future research and could guide efforts to develop novel augmentation strategies for antidepressant treatment resistant individuals. 38 samples, 2 dentate regions (dorsal/ventral), 3 groups (control, antidepressant resistant (4 mice), antidepressant responsive (7 mice), untreated (8 mice).
2013-12-31 | E-GEOD-43261 | biostudies-arrayexpress
Project description:To explored the mechanism of pharmacokinetic perturbation in chronic unpredicted mild stress (CUMS) resulting depression, CUMS-induced depression animal model with spontaneous diabetic GK rats were established. The expression profile in GK rats' livers were screened using Affymetrix Rat 230 2.0 Array.
2017-09-25 | GSE94988 | GEO