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

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

PROVIDER: PRJNA614639 | 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:Poly(I:C)-induced long-term behavioral deficits are accompanied by epigenetic changes in microglia of male mice (ChIP-seq)

| PRJNA614640 | ENA

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: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

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

| PRJNA811237 | ENA

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

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

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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

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RNAseq data for FACS sorted glial cells KPNA4 KO mice for Importin α4 deficiency induces psychiatric disorder-related behavioral deficits and neuroinflammation in mice.

Project description:Importin α4, which is encoded by the Kpna4 gene, is a well characterized nuclear-cytoplasmic transport factor known to mediate transport of transcription factors including NF-κB. Here, we report that Kpna4 knock-out (KO) mice exhibit psychiatric disorder-related behavioral abnormalities such as anxiety-related behaviors, deceased social interaction and sensorimotor gating deficits. Contrary to a previous study predicting attenuated NF-κB activity as a result of Kpna4 deficiency, we observed a significant increase in expression levels of NF-κB genes and pro-inflammatory cytokines such as TNFα, Il1β or Il-6 in the Prefrontal Cortex or Basolateral Amygdala of the KO mice. Moreover, examination of inflammatory responses in primary cells revealed that Kpna4 deficient cells have an increased inflammatory response, which was rescued by addition of not only full-length, but also a nuclear transport deficient truncation mutant of importin α4, suggesting contribution of its non-transport functions. Furthermore, RNAseq of sorted adult Microglia and Astrocytes and subsequent transcription factor analysis suggested increases in Polycomb repressor complex 2 (PRC2) activity in Kpna4 KO cells. Taken together, importin α4 deficiency induces psychiatric disorder-related behavioral deficits in mice, along with an increased inflammatory response and possible alteration of PRC2 activity in glial cells.

2024-04-18 | GSE264180 | GEO

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