Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1082091 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28161550.fastq.gz | Fastqsanger.gz | |||
| SRR28161551.fastq.gz | Fastqsanger.gz | |||
| SRR28161552.fastq.gz | Fastqsanger.gz | |||
| SRR28161553.fastq.gz | Fastqsanger.gz | |||
| SRR28161554.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 31 |
Similar Datasets
Project description:The deficiency of n-3 PUFAs in the brain and depressive symptoms are closely related. Krill oil contains abundant amounts of n-3 PUFAs incorporated in phosphatidylcholine.However, the effect of krill oil treatment on depression-like behaviors induced by chronic stress and its molecular mechanism in the brain remain poorly understood. Here, we used a chronic unpredictable mild stress (CUMS) model to evaluate the effect of krill oil on depression-like behaviors and explored its molecular mechanism through lipid metabolomics and mRNA profiles in the whole brain.
2023-07-19 | GSE237760 | 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:Major depressive disorder (MDD) is a highly heterogeneous psychiatric disorder. The pathogenesis of MDD remained unclear, and it may be associated with exposure to different stressors. Most previous studies have focused on molecular changes in a single stress-induced depression model, which limited the identification of the pathogenesis of MDD. The depressive-like behaviors were induced by four well-validated stress models in rats, including chronic unpredictable mild stress, learned helplessness stress, chronic restraint stress and social defeat stress. We applied proteomic to investigate molecular changes in the hippocampus of those four models and revealed 529 proteins.
2023-05-22 | PXD043285 |
Project description:Stressful life events increase risk for depression, yet the molecular mechanisms by which stress is encoded in the brain to induce maladaptive behaviors are not well understood. Emerging evidence has shown that stress dysregulates gene expression in the brain, yet the cellular origin of these gene expression alterations has yet to be determined. To address this question, we used a chronic unpredictable stress (CUS) paradigm that drives depressive- and anxiety-like behaviors in male and female mice and single-nucleus transcriptomics to identify cell type-specific gene expression changes in the cortex. We find that neocortical excitatory neurons are particularly vulnerable to chronic stress exposure, and that CUS reprograms these cells to decrease transcription of synaptic genes involved in glutamatergic neurotransmission. We identify the ubiquitously expressed factor, Yin Yang 1 (YY1), as a key driver of the transcriptional reprogramming observed in excitatory neurons isolated from CUS mice. Selective depletion of YY1 in excitatory neurons of the prefrontal cortex (PFC) increases the stress sensitivity of mice, inducing depressive- and anxiety-related behaviors following an abbreviated stress exposure and deregulating expression of key stress-related genes in the PFC. Importantly, we find that YY1 functions in both males and females to facilitate stress coping. This work establishes a novel mechanism underlying chronic stress-induced behavior, in which epigenetic responses to stress in PFC excitatory neurons are mediated by stress-dependent YY1 activity. Our findings demonstrate how post-mitotic neurons adapt to stress experience and identify a novel molecular target that is generalizable to males and females for therapeutic treatment of stress-related neuropsychiatric disorders.
2021-11-19 | GSE145970 | GEO
Project description:Major depressive disorder (MDD) is a prevalent and life-threatening illness in modern society. The susceptibility to MDD is profoundly influenced by environmental factors, such as stressful lifestyle or traumatic events, which could impose maladaptive transcriptional program through epigenetic regulation. However, the underlying molecular mechanisms remain elusive. Here we report that stress-susceptible rodents exhibit lower levels of histone crotonylation in the medial prefrontal cortex (mPFC), concurrent with regional upregulation of chromodomain Y-like (CDYL), a crotonyl-CoA hydratase and histone methyllysine reader. Overexpression of CDYL in the prelimbic cortex (PL), a sub-region of mPFC, increases microdefeat-induced social avoidance behaviors and anhedonia in mice. Conversely, knockdown of CDYL in PL prevents chronic social defeat stress-induced depression-like behaviors. Mechanistically, we show that CDYL inhibits structural synaptic plasticity mainly by transcriptional repression of neuropeptide VGF, and this activity is dependent on its dual effect on regional histone crotonylation and H3K27 tri-methylation on the VGF promoter. Together, our data indicate CDYL plays a critical role in regulating stress-induced depression-like behaviors, providing a potential therapeutic target for MDD.
2018-11-15 | GSE120293 | 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:Synbiotics are a combination of probiotics and prebiotics which can alter the composition of the gastrointestinal tract evoking beneficial effects throughout the body through the production of a battery of bioactive metabolites. In this study, a synbiotic was used to reduce the behavioral and biochemical symptoms of depression and this nanostring panel was used to decipher where along the gut-brain-axis the synbiotic-derived metabolites were invoking their beneficial effects on the immune system. The synbitoic was composed of two probiotic bacteria (Lactobacillus fermentum ATCC 793 and Bifidobacteria longum ATCC 15707 and a grape -derived prebiotic composed of grape seed polyphenol extract, resveratrol and a concord grape extract. Male mice (C57BL/6) were pretreatment with either nothing (control), BDPP, probiotic or synbiotic and underwent 28 days of chronic unpredicitable stress. After 28 days, animals' behavior reflected an increase in depressive- and anxiety-like behavior, rescued specifically by the synbiotic. This nanostring multiplex analysis reveals both tissue- and treatment-specific effects on immune modulators.
2020-11-03 | GSE148579 | GEO
Project description:Human major depressive disorder (MDD), along with related mood disorders, is among the world’s greatest public health concerns, however, its pathophysiology remains poorly understood. Persistent changes in gene expression are known to promote physiological aberrations implicated in MDD. More recently, histone mechanisms affecting cell-type and regional specific chromatin structures have also been shown to contribute to transcriptional programs related to depressive behaviors, as well as responses to antidepressants (ADs). Although much emphasis has been placed in recent years on roles for histone posttranslational modifications (PTMs) and chromatin remodeling events in the etiology of MDD, it has become increasingly clear that replication-independent histone variants (e.g., H3.3), which differ in primary amino acid sequence from their canonical counterparts, similarly play critical roles in the regulation of activity-dependent neuronal transcription, synaptic connectivity and behavioral plasticity. Here, we demonstrate a novel role for increased H3.3 dynamics in nucleus accumbens (NAc)––a key limbic brain reward region––in the regulation of aberrant social stress-mediated gene expression, abnormal dendritic morphology and the precipitation of depressive-like behaviors in mice. We find that molecular blockade of these dynamics promotes resilience to chronic social stress and results in a partial re-normalization of stress-associated transcriptional patterns in NAc. In sum, our findings establish H3.3 dynamics as a critical, and previously undocumented, regulator of mood, and suggest that future therapies aimed at modulating striatal histone dynamics may potentiate beneficial behavioral adaptations to negative emotional stimuli.
2017-02-08 | GSE85900 | GEO
Project description:Chronic stress induces adaptive changes in the brain via the cumulative action of glucocorticoids, which is associated with mood disorders. Here we show that repeated daily five-minute restraint resolves pre-existing stress-induced depressive-like behavior in mice. Repeated injection of glucocorticoids in low doses mimics the anti-depressive effects of short-term stress. Repeated exposure to short-term stress and injection of glucocorticoids activate neurons in largely overlapping regions of the brain, as shown by c-Fos staining, and reverse distinct stress-induced gene expression profiles. Chemogenetic inhibition of neurons in the prelimbic cortex projecting to the nucleus accumbens, basolateral amygdala, or bed nucleus of the stria terminalis results in anti-depressive effects similarly to short-term stress exposure, while only inhibition of neurons in the prelimbic cortex projecting to the bed nucleus of the stria terminalis rescues glucocorticoid release. In summary, we show that short-term stress can reverse adaptively altered stress gains and resolve stress-induced depressive-like behavior.
2021-09-09 | GSE183624 | GEO