Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Reduced Brd1 expression leads to reversible depression-like behaviors and gene-expression changes in female mice

ABSTRACT: Reduced Brd1 expression leads to reversible depression-like behaviors and gene-expression changes in female mice

PROVIDER: PRJNA631687 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11780704.fastq.gz	Fastqsanger.gz
	SRR11780705.fastq.gz	Fastqsanger.gz
	SRR11780706.fastq.gz	Fastqsanger.gz
	SRR11780707.fastq.gz	Fastqsanger.gz
	SRR11780708.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 115

Similar Datasets

Reduced Brd1 expression leads to reversible depression-like behaviors and gene-expression changes in female mice [amygdala]

Project description:Background: The schizophrenia associated gene, BRD1, encodes an epigenetic regulator which chromatin interactome is enriched with genes implicated in mental health. Alterations in histone modifications and epigenetic regulation contribute to brain transcriptomic changes in affective disorders and preclinical data supports a role for BRD1 in psychopathology. However, the implications of BRD1 on affective pathology remains poorly understood. Methods: We assessed affective behaviors and associated neurobiology in Brd1+/- mice along with their responses to Fluoxetine and Imipramine. This involves behavioral, neurostructural, and neurochemical characterizations along with regional cerebral gene expression profiling combined with integrative functional genomic analyses. Results: Here we report behavioral changes in female Brd1+/- mice with translational value to depressive symptomatology that can be alleviated by administration of antidepressant medications. Behavioral changes are accompanied by altered brain morphometry and imbalances in monoaminergic systems. In accordance, gene expression changes across brain tissues reveal altered neurotransmitter signaling and cluster in functional pathways associated with depression including ‘Adrenergic-, GPCR-, cAMP-, and CREB/CREM-signaling’. Integrative gene expression analysis specifically links changes in amygdaloid intracellular signaling activity to the behavioral treatment response in Brd1+/- mice. Conclusions: Collectively, our study highlights the importance of BRD1 as a modulator of affective pathology and adds to our understanding of the molecular mechanisms underlying affective disorders and their treatment response.

2020-06-20 | GSE150431 | GEO

Reduced Brd1 expression leads to reversible depression-like behaviors and gene-expression changes in female mice [Striatum (CPu)]

2020-06-20 | GSE150028 | GEO

Reduced Brd1 expression leads to reversible depression-like behaviors and gene-expression changes in female mice [anterior cingulate cortex (aCC)]

2020-06-20 | GSE150264 | GEO

Reduced Brd1 expression leads to reversible depression-like behaviors and gene-expression changes in female mice [amygdala]

Project description:Reduced Brd1 expression leads to reversible depression-like behaviors and gene-expression changes in female mice [amygdala]

| PRJNA632028 | ENA

Reduced Brd1 expression leads to reversible depression-like behaviors and gene-expression changes in female mice [Striatum (CPu)]

Project description:Reduced Brd1 expression leads to reversible depression-like behaviors and gene-expression changes in female mice [Striatum (CPu)]

| PRJNA630955 | ENA

Reduced Brd1 expression leads to reversible depression-like behaviors and gene-expression changes in female mice [anterior cingulate cortex (aCC)]

Project description:Reduced Brd1 expression leads to reversible depression-like behaviors and gene-expression changes in female mice [anterior cingulate cortex (aCC)]

| PRJNA631693 | ENA

Reduced Brd1 expression leads to reversible depression-like behaviors and gene-expression changes in female mice.

Project description:The schizophrenia-associated gene, BRD1, encodes an epigenetic regulator in which chromatin interactome is enriched with genes implicated in mental health. Alterations in histone modifications and epigenetic regulation contribute to brain transcriptomic changes in affective disorders and preclinical data supports a role for BRD1 in psychopathology. However, the implication of BRD1 on affective pathology remains poorly understood. In this study, we assess affective behaviors and associated neurobiology in Brd1+/- mice along with their responses to Fluoxetine and Imipramine. This involves behavioral, neurostructural, and neurochemical characterizations along with regional cerebral gene expression profiling combined with integrative functional genomic analyses. We report behavioral changes in female Brd1+/- mice with translational value to depressive symptomatology that can be alleviated by the administration of antidepressant medications. Behavioral changes are accompanied by altered brain morphometry and imbalances in monoaminergic systems. In accordance, gene expression changes across brain tissues reveal altered neurotransmitter signaling and cluster in functional pathways associated with depression including 'Adrenergic-, GPCR-, cAMP-, and CREB/CREM-signaling'. Integrative gene expression analysis specifically links changes in amygdaloid intracellular signaling activity to the behavioral treatment response in Brd1+/- mice. Collectively, our study highlights the importance of BRD1 as a modulator of affective pathology and adds to our understanding of the molecular mechanisms underlying affective disorders and their treatment response.

| S-EPMC7367888 | biostudies-literature

Reduced Brd1 expression leads to reversible depression-like behaviors and gene-expression changes in female mice

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-06-20 | GSE150265 | GEO

Hyperactive lateral habenula mediates the comorbidity between rheumatoid arthritis and depression-like behaviors

Project description:Objective: The aim of this study was to identify the neural and molecular mechanisms underlying the comorbidity of rheumatoid arthritis (RA) and depression. Methods: A cohort of 200 RA patients were recruited to quantitatively assess the association between depressive symptoms and RA disease activity, as well as quality of life. The collagen antibody-induced arthritis (CAIA) mouse model of RA was used to screen for brain regions that showed changes in c-FOS expression, an indicator of alteration in brain activity, accompanying the appearance of depression-like behaviors. RNA sequencing, immunostaining, AAV-mediated expression, micro-CT, plasma cytokines/chemokines measurements and histological analyses were applied to evaluate the contribution of the identified brain region in the disease progression of RA and depression-like symptoms. Results: In this study, we showed that in RA patients, the depression scores were significantly correlated with the severity and quality of life of the patients. The CAIA mice developed RA symptoms, together with depression-like behaviors accompanied by hyperactivity and alterations in gene expression reflecting cerebrovascular disruption in the lateral habenula (LHb), a brain region processing negative valence. Importantly, inhibition of the LHb outputs not only alleviated depression-like behaviors, but also resulted in rapid remission of RA symptoms and reduction in sympathetic nerve fibers in the synovial joints of the CAIA mice.Conclusion: Our study highlights a critical but previously overlooked contribution of hyperactive LHb to the comorbidity between RA and depression, suggesting that targeting LHb in conjunction with RA treatments may be a promising strategy for RA patients comorbid with depression.

2025-08-30 | GSE241929 | GEO

A pancreas–hippocampus feedback mechanism regulates circadian changes in depression-related behaviors

Project description:Individuals with neuropsychiatric disorders often show metabolic symptoms. However, the mechanisms underlying this co-occurrence remain unclear. Here, we show that iPSC-derived pancreatic islets from individuals with bipolar disorder (BD) have insulin secretion deficits caused by increased expression of RORβ, a susceptibility gene for BD. Enhancing RORβ expression in mouse pancreatic β-cells induced depression-related behaviors in the light phase and mania-like behaviors in the dark phase. Pancreatic RORβ overexpression in the light phase reduced insulin release from islets, inducing hippocampal hyperactivity and depression-like behaviors. Further, this hippocampal hyperactivity in the light phase had the delayed effect of promoting insulin release in the dark phase, resulting mania-like behaviors and hippocampal neuronal hypoactivity. Our results in mice point to a pancreas–hippocampus feedback mechanism by which metabolic and circadian factors cooperate to generate behavioral fluctuations and which may play a role in bipolar disorder.

2024-12-01 | GSE283118 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data