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Extensive sex differences in depression-linked variants functionally assayed in mouse brain [Hippocampus]

ABSTRACT: Extensive sex differences in depression-linked variants functionally assayed in mouse brain [Hippocampus]

PROVIDER: PRJNA773474 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16524962.fastq.gz	Fastqsanger.gz
	SRR16524963.fastq.gz	Fastqsanger.gz
	SRR16524964.fastq.gz	Fastqsanger.gz
	SRR16524965.fastq.gz	Fastqsanger.gz
	SRR16524966.fastq.gz	Fastqsanger.gz

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Extensive sex differences in depression-linked variants functionally assayed in mouse brain [Hippocampus]

Project description:Here, we selected >1000 variants from over 30 depression-associated loci using brain epigenomic data, and functionally assayed them using in vivo functional assays in the mouse brain to examine sex-by-genotype interactions. We identify extensive sex-by-allele effects in mature hippocampus, suggesting genetic risk and thus disease mechanisms may be distinct between the sexes. Unbiased informatics approaches indicated a role for nuclear hormone receptors, which was supported by . Further, comparative analysis of allelic function in the neonatal mouse brain, during a key between developmental neonates during the masculinizing testosterone surge, and in the adult hippocampus—a region of interest in depression pathology—but not at 10 days old, a older hormonally quiescent developmental stage juveniles. Our study provides novel insights into depression genetics as influenced by age, biological sex, and cell type, and provides a framework for in vivo parallel assays at a scale not previously shown possible to functionally define interactions between sex and disease variation.

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Extensive sex differences in depression-linked variants functionally assayed in mouse brain [Hippocampus II]

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Extensive sex differences in depression-linked variants functionally assayed in mouse brain

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Extensive sex differences in depression-linked variants functionally assayed in mouse brain [Hippocampus II]

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Extensive sex differences in depression-linked variants functionally assayed in mouse brain [P0&P10]

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Extensive sex differences in depression-linked variants functionally assayed in mouse brain [P0&P10]

Project description:Extensive sex differences in depression-linked variants functionally assayed in mouse brain [P0&P10]

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Extensive sex differences in depression-linked variants functionally assayed in mouse brain

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

2023-02-10 | GSE186348 | GEO

Expression data from the hippocampus of LPS induced depression mice model treated with Luteolin

Project description:Gene expression profiling reveals a potential role of Luteolin in LPS induced depression model LPS depression induced mice were orally treated with luteolin (10 mg/kg body weight) once per day during 8 consecutive days. Microarray gene expression was conducted on mice hippocampal tissues. Two mice brains were used for each expermient . The Microarray gene expression was conducted on hipocampus from LPS depression induced mice model(LPS group), LPS depression induced mice model treated with luteolin(LPS+L group), Normal mice (PBS group) and Normal mice treated with luteolin (PBS+L).

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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.

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