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Poly(I:C)-induced long-term behavioral deficits are accompanied by epigenetic changes in microglia of male mice (ChIP-seq)

ABSTRACT: Poly(I:C)-induced long-term behavioral deficits are accompanied by epigenetic changes in microglia of male mice (ChIP-seq)

PROVIDER: PRJNA614640 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11401919_1.fastq.gz	Fastqsanger.gz
	SRR11401919_2.fastq.gz	Fastqsanger.gz
	SRR11401920_1.fastq.gz	Fastqsanger.gz
	SRR11401920_2.fastq.gz	Fastqsanger.gz
	SRR11401921_1.fastq.gz	Fastqsanger.gz

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Poly(I:C)-induced long-term behavioral deficits are accompanied by epigenetic changes in microglia of male mice (ChIP-seq)

Project description:While the exact mechanisms for a sex bias in the development of neuropsychiatric disorders remain only vaguely understood, there is increasing evidence that an early life immune activation contributes to the disease pathogenesis. By administering the double stranded RNA analogue polyriboinosinic:polyribocytidilic acid (poly(I:C)) we mimicked an early viral infection in neonatal female and male mice. As a consequence, male adolescent mice presented long-term behavioral deficits including impaired social behavior and defective spatial working and recognition memory. Notably, behavioral changes were completely absent in female mice. In male mice, poly(I:C) led to an increased number of infiltrating T cells in the brain parenchyma, an enhanced interferon-g (IFNg) signaling, and an epigenetic reprogramming of microglial cells. These reprogrammed microglial cells showed increased phagocytic activity, which resulted in the excessive loss of dendritic spines in male mice only. We corroborated these findings in a murine neonatal infection of mice with murine cytomegalovirus (MCMV) and found sustained aversive behavioral effects and a lower number of excitatory synapses within the hippocampal brain region in young adult male, but not in female mice. Together, our results highlight the crucial role of the early postnatal period for normal brain development: identical immune stimulation during this period led to distinct sex-specific long-term behavioral deficits, indicating that sex is potentially an underappreciated factor when investigating neuropsychiatric disorders.

2023-03-24 | GSE147443 | GEO

Poly(I:C)-induced long-term behavioral deficits are accompanied by epigenetic changes in microglia of male mice

Project description:Poly(I:C)-induced long-term behavioral deficits are accompanied by epigenetic changes in microglia of male mice

| PRJNA614639 | ENA

Poly(I:C)-induced long-term behavioral deficits are accompanied by epigenetic changes in microglia of male mice

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

2023-03-24 | GSE147444 | GEO

Impairment of methylglyoxal detoxification systems causes mitochondrial dysfunction and behavioral deficits

Project description:Methylglyoxal (MG) is a reactive alpha-dicarbonyl by-product of glycolysis. Several bio-defense systems to detoxify the highly toxic MG are equipped in our body, including an enzymatic system by glyoxalase (GLO) 1 and GLO2 and a scavenge system by vitamin B6 (VB6). We have reported that some population of patients with schizophrenia shows impairment of the MG detoxification systems. Although we have evidences showing a link between impairment of MG detoxification systems and development of schizophrenia, the molecular mechanism to connect them remains poorly understood. Here, we generated a novel mouse model for MG detoxification deficits by feeding Glo1 knockout mice with VB6-lacking diets (KO/VB6(-)), and evaluate effects of impaired MG detoxification systems on brain function. KO/VB6(-) mice showed the accumulation of MG in the prefrontal cortex (PFC), hippocampus, and striatum, and displayed schizophrenia-like behavioral deficits, such as social deficits, cognitive impairment, a sensorimotor deficit in the prepulse inhibition test. Furthermore, we found aberrant gene expression related to mitochondria function in the PFC of the KO/VB6(-) mice by RNA-seq and weighted gene correlation network analysis (WGCNA). Finally, we actually demonstrated respiratory deficits in mitochondria isolated from the PFC of KO/VB6(-) mice. These findings suggest that MG detoxification deficits might cause schizophrenia-like behavioral deficits via mitochondrial dysfunction in the PFC.

2021-07-20 | GSE149585 | GEO

Impairment of methylglyoxal detoxification systems causes mitochondrial dysfunction and behavioral deficits

Project description:Impairment of methylglyoxal detoxification systems causes mitochondrial dysfunction and behavioral deficits

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Loss of neuronal 3D chromatin organization causes transcriptional and behavioral deficits related to serotonergic dysfunction

Project description:The interior of the eukaryotic cell nucleus is a highly organized 3D structure. In mature hippocampal and cortical pyramidal neurons, transcriptionally silent DNA is typically compacted in a few clusters referred to as chromocenters that are strongly stained with DNA intercalating agents like DAPI and whose function is still uncertain. We found that this 3D structure was severely disrupted by the incorporation of the chimeric histone H2BGFP into neuronal chromatin. Experiments in inducible and forebrain restricted bitransgenic mice demonstrated that the expression of this histone alters the higher-order organization of neuronal heterochromatin and causes a complex behavioral phenotype that includes hyperactivity, and social interaction, prepulse inhibition and cognitive defects. This phenotype was associated with highly specific transcriptional deficits that affected several serotonin receptor genes located at the edge of gene desert regions. Pharmacological and electrophysiological experiments indicate that this epigenetically-induced hyposerotonergic state may underlie the behavioral defects. Our results suggest a new role for perinuclear heterochromatin and chromocenter organization in the epigenetic regulation of neuronal gene expression and mental illness. We used microarrays to detect differential gene expression in transgenic mice expressing histone H2BGFP in the forebrain. We obtained triplicate samples (biological replicates) of either genotype (wild-type and H2BGFP mice). Each sample contained pooled total RNA from the hippocampi of 2 three-month old genotype-matched mice.

2014-07-18 | E-GEOD-48437 | biostudies-arrayexpress

Epigenetic Treatment of Behavioral and Physiological Deficits in a Tauopathy Mouse Model

Project description:Epigenetic Treatment of Behavioral and Physiological Deficits in a Tauopathy Mouse Model

| PRJNA755255 | ENA

Gut Microbiota from Human Autism Spectrum Disorder Induces Behavioral Deficits in Mice

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Transcriptomic and long-term behavioral deficits associated with developmental 3.5 GHz radiofrequency radiation exposures in zebrafish

Project description:Transcriptomic and long-term behavioral deficits associated with developmental 3.5 GHz radiofrequency radiation exposures in zebrafish

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Long-term caffeine treatment of Alzheimer mouse models ameliorates behavioural deficits and neuron loss and promotes cellular and molecular markers of neurogenesis

Project description:Epidemiological studies suggest that consumption of caffeine, the most commonly consumed psychoactive substances found in coffee, tea or soft drinks reduces the risk of developing Alzheimer’s disease (AD). While previous studies employing transgenic AD mouse models reported on reduced amyloid plaque load or an amelioration of behavioral deficits, there is only limited information on its potential effects on neurodegeneration. In the current study, we assessed whether long-term caffeine consumption affects hippocampal neuron loss and associated behavioral deficits in the Tg4-42 mouse model of AD. Treatment over a 4 months period reduced hippocampal neuron loss, rescued learning and memory deficits and ameliorates impaired neurogenesis. Neuron-specific hippocampal transcriptome analysis revealed an altered expression profile with an up-regulation of genes linked to synaptic function and processes, as well as neural progenitor proliferation. Treatment of 5xFAD mice with the same paradigm also rescued behavioral deficits, however, without affecting extracellular amyloid-beta (Abeta) levels or altered APP processing.

2021-12-13 | GSE183323 | GEO

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