Ontology highlight
ABSTRACT:
PROVIDER: PRJNA890941 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21922100_1.fastq.gz | Fastqsanger.gz | |||
| SRR21922100_2.fastq.gz | Fastqsanger.gz | |||
| SRR21922101_1.fastq.gz | Fastqsanger.gz | |||
| SRR21922101_2.fastq.gz | Fastqsanger.gz | |||
| SRR21922102_1.fastq.gz | Fastqsanger.gz |
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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:Accumulating evidence demonstrates that the gut microbiota affects brain function and behavior, including depressive behavior. Antidepressants are the main drugs used for treatment of depression. We hypothesized that antidepressant treatment could modify gut microbiota which can partially mediate their antidepressant effects. Mice were chronically treated with one of five antidepressants (fluoxetine, escitalopram, venlafaxine, duloxetine or desipramine), and gut microbiota was analyzed, using 16s rRNA gene sequencing. After characterization of differences in the microbiota, chosen bacterial species were supplemented to vehicle and antidepressant-treated mice, and depressive-like behavior was assessed to determine bacterial effects. RNA-seq analysis was performed to determine effects of bacterial treatment in the brain. Antidepressants reduced richness and increased beta diversity of gut bacteria, compared to controls. At the genus level, antidepressants reduced abundances of Ruminococcus, Adlercreutzia, and an unclassified Alphaproteobacteria. To examine implications of the dysregulated bacteria, we chose one of antidepressants (duloxetine) and investigated if its antidepressive effects can be attenuated by simultaneous treatment with Ruminococcus flavefaciens or Adlercreutzia equolifaciens. Supplementation with R. flavefaciens diminished duloxetine-induced decrease in depressive-like behavior, while A. equolifaciens had no such effect. R. flavefaciens treatment induced changes in cortical gene expression, up-regulating genes involved in mitochondrial oxidative phosphorylation, while down-regulating genes involved in neuronal plasticity. Our results demonstrate that various types of antidepressants alter gut microbiota composition, and further implicate a role for R. flavefaciens in alleviating depressive-like behavior.
2019-04-05 | GSE129359 | GEO
Project description:The depressive-like behavior in animals is usually assessed by standardized behavioral tests such as the forced swimming test. However, the findings of these tests may be affected by individual variability among animals, which may hinder the discovery of genes responsible for depression. Few reports have showed the influence of individual variability in identifying the genes associated with depressive-like behavior. In this study, we measured the immobility ratio (% immobility in 5 min) in the forced swimming test in 106 male Wistar rats. According to the distribution of individual immobility ratio, the rats were divided into three groups: the control group with immobility ratio -1 to +1 standard deviation (SD) from the mean, the depressive group with immobility ratio +1 to +2 SD above the mean, and the anti-depressive group with immobility ratio -1 to -2 SD below the mean. Microarray analysis was used to identify the genes differentially expressed by depressive group rats in the prefrontal cortex and cerebellum. The differentially expressed genes in both brain regions of the depressive group were Alas2, Gh1, Hba-a2, Hbb, Hbb-b1, Hbe2, LOC689064, Mrps10, Mybpc, Olf6415, and Pfkb1. Ingenuity pathway analysis identified Gh1 as a hub gene in the networks of the differentially expressed genes in both brain regions. This study indicates that inherent differences in depressive-like behavior may be related to the Gh1 expression in the cerebellum and prefrontal cortex. We measured the immobility ratio of 106 normal rats using the forced swimming test and statistically analysis. We selected the rats exhibitting depressive-like behavior or average in the 106 rats. Total RNA was prepareted from the cerebellum and prefrontal cortex. An equal amount of RNA from 4 rats in each group was pooled and used for microarray analysis.
2015-02-26 | E-GEOD-63377 | biostudies-arrayexpress
Project description:Major depressive disorder (MDD) is the psychiatric disorder with the highest prevalence in the world. Pharmacological antidepressant treatment (AD), such as selective serotonin reuptake inhibitors [SSRI, i.e. fluoxetine (Flx)] is the first line of treatment for MDD. Despite its efficacy, lack of AD response occurs in numerous patients characterizing Difficult-to-treat Depression. ElectroConvulsive Therapy (ECT) is a highly effective treatment inducing rapid improvement in depressive symptoms and high remission rates of ~50–63% in patients with pharmaco-resistant depression. Nevertheless, the need to develop reliable treatment response predictors to guide personalized AD strategies and supplement clinical observation is becoming a pressing clinical objective. Here, we propose to establish a proteomic peripheral biomarkers signature of ECT response in an anxio/depressive animal model of non-response to AD. Using an emotionality score based on the analysis complementary behavioral tests of anxiety/depression (Elevated Plus Maze, Novelty Suppressed Feeding, Splash Test), we showed that a 4-week corticosterone treatment (35 μg/ml, Cort model) in C57BL/6JRj male mice induced an anxiety/depressive-like behavior. A 28-days chronic fluoxetine treatment (Flx, 18 mg/kg/day) reduced corticosterone-induced increase in emotional behavior. A 50% decrease in emotionality score threshold before and after Flx, was used to separate Flx-responding mice (Flx-R, n=18), or Flx non-responder mice (Flx-NR, n=7). Then, Flx-NR mice received 7 sessions of electroconvulsive seizure (ECS, equivalent to ECT in humans) and blood was collected before and after ECS treatment. Chronic ECS normalized the elevated emotionality observed in Flx-NR mice. Then, proteins were extracted from peripheral blood mononuclear cells (PBMCs) and isolated for proteomic analysis using a high-resolution MS Orbitrap. The proteomic analysis revealed a signature of 33 peripheral proteins associated with response to ECS (7 down- and 26 upregulated). These proteins were previously associated with mental disorders and involved in regulating pathways which participate to the depressive disorder etiology. remark for sample name : ECTR=Flx-NR-ES, C=cort/Veh, CFNR= Flx-NR
2022-11-01 | PXD037392 | Pride
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.
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Project description:The depressive-like behavior in animals is usually assessed by standardized behavioral tests such as the forced swimming test. However, the findings of these tests may be affected by individual variability among animals, which may hinder the discovery of genes responsible for depression. Few reports have showed the influence of individual variability in identifying the genes associated with depressive-like behavior. In this study, we measured the immobility ratio (% immobility in 5 min) in the forced swimming test in 106 male Wistar rats. According to the distribution of individual immobility ratio, the rats were divided into three groups: the control group with immobility ratio -1 to +1 standard deviation (SD) from the mean, the depressive group with immobility ratio +1 to +2 SD above the mean, and the anti-depressive group with immobility ratio -1 to -2 SD below the mean. Microarray analysis was used to identify the genes differentially expressed by depressive group rats in the prefrontal cortex and cerebellum. The differentially expressed genes in both brain regions of the depressive group were Alas2, Gh1, Hba-a2, Hbb, Hbb-b1, Hbe2, LOC689064, Mrps10, Mybpc, Olf6415, and Pfkb1. Ingenuity pathway analysis identified Gh1 as a hub gene in the networks of the differentially expressed genes in both brain regions. This study indicates that inherent differences in depressive-like behavior may be related to the Gh1 expression in the cerebellum and prefrontal cortex.
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Project description:Genome-wide MeDIP-Sequencing of 23 monozygotic twin pairs (n=46) from Australia discordant for major depressive disorder (MDD). MeDIP-seq of 23 monozygotic twin pairs discordant for major depressive disorder. MZ twin pairs were compared to identify significantly differently methylated sites associated with MDD.
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Project description:Genome-wide MeDIP-Sequencing was carried out on a total of 50 monozygotic twin pairs from the UK and Australia that are discordant for depression. We show that major depressive disorder is associated with significant hypermethylation within the coding region of ZBTB20, and is replicated in an independent cohort of 356 unrelated case-control individuals. The twins with major depressive disorder also show increased global variation in methylation in comparison with their unaffected co-twins. ZBTB20 plays an essential role in the specification of the Cornu Ammonis-1 field identity in the developing hippocampus, a region previously implicated in the development of major depressive disorder. Epigenetic study of MZ twins discordant for Major Depressive Disorder
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Project description:Depression is one of the most common neuropsychiatric disorders. Although the pathogenesis of depression is still unknown, environmental risk factors and genetics are implicated. Copper (Cu), a cofactor of multiple enzymes, is involved in regulating depression-related processes. Depressed patients carrying the apolipoprotein ε4 allele display more severe depressive symptoms, indicating that ApoE4 is closely associated with an increased risk of depression. The study explored the effect of low-dose Cu (0.13 ppm) exposure and ApoE4 on depression-like behavior of mice and further investigate the possible mechanisms. The 4-month-old ApoE4 mice and wild-type (WT) mice were treated with 0.13 ppm CuCl2 for 4 months. After the treatment, ApoE4 mice displayed obvious depression-like behavior compared with the WT mice, and Cu exposure further exacerbated the depression-like behavior of ApoE4 mice. There was no significant difference in anxiety behavior (Open field test) and memory behavior (Morris water maze). Proteomic analysis revealed that the differentially expressed proteins between Cu-exposed and non-exposed ApoE4 mice were mainly involved in Ras signaling pathway, protein export, axon guidance, serotonergic synapse, GABAergic synapse, dopaminergic synapse. Among these differentially expressed proteins, immune response and synaptic function are highly correlated. Representative protein expression changes are quantified by Western blot, showing consistent results as determined by proteomic analysis. Hippocampal astrocytes and microglia were increased in Cu-exposed ApoE4 mice, suggesting that neuroglial cells played an important role in the pathogenesis of depression. Taken together, our study demonstrated that Cu exposure exacerbates depression-like behavior of ApoE4 mice and the mechanisms may involve the dysregulation of synaptic function and immune response, and overactivation of neuroinflammation.
2021-09-09 | PXD022422 | Pride
Project description:Background: As a worldwide threat to mental health, depression affects about 322 million people globally. Recently, the role of gut microbiota dysbiosis on the pathogenesis of depression has received widespread attention, but the underlying mechanism remains elusive.Results: Corticosterone (CORT)-treated mice showed depressive-like behaviors, a reduction in hippocampal neurogenesis, and an altered composition of gut microbiota (GM). Fecal microbial transplantation (FMT) from CORT-treated mice transferred depressive-like phenotypes and their dominant GM, especially bifidobacterium and lactobacillus, to the recipients. Fecal metabolic profiling showed that the relative abundances of fecal ceramides were significantly increased in CORT-treated and the recipient mice. Metagenomic sequencing exposed that bifidobacterium and lactobacillus might be responsible for gut ceramides production in CORT-treated mice. We then found that treatment with ceramides via oral gavage was sufficient to recapitulate the depressive-like phenotypes in wild -type mice. Finally, RNA-sequencing data exposed that most of the differentially expressed genes (DEGs) between ceramides-treated mice and the control group were enriched in oxidative phosphorylation (OXPHOS) pathway. Conclusion: We conclude that chronic exposure to CORT leads to an altered GM composition and consequent ceramides production, thus leading to subtle mitochondrial OXPHOS dysfunction in hippocampus, which may contribute to the development of depressive disorders.
2024-04-01 | GSE229237 | GEO