Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Maternal immune activation impairs cognitive flexibility and alters transcription in frontal cortex

ABSTRACT: We examined mRNA expression differences in frontal cortex of adult offspring of Poly(I:C)- and Saline-exposed mice

ORGANISM(S): Mus musculus

PROVIDER: GSE137497 | GEO | 2019/09/17

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Maternal immune activation impairs cognitive flexibility and alters transcription in frontal cortex.

Project description:BACKGROUND:Epidemiological studies suggest that the risk of neurodevelopmental disorders such as autism spectrum disorder (ASD) and schizophrenia is increased by prenatal exposure to viral or bacterial infection during pregnancy. It is still unclear how activation of the maternal immune response interacts with underlying genetic factors to influence observed ASD phenotypes. METHODS:The current study investigated how maternal immune activation (MIA) in mice impacts gene expression in the frontal cortex in adulthood, and how these molecular changes relate to deficits in cognitive flexibility and social behavior, and increases in repetitive behavior that are prevalent in ASD. Poly(I:C) (20 mg/kg) was administered to dams on E12.5 and offspring were tested for social approach behavior, repetitive grooming, and probabilistic reversal learning in adulthood (n = 8 vehicle; n = 9 Poly(I:C)). We employed next-generation high-throughput mRNA sequencing (RNA-seq) to comprehensively investigate the transcriptome profile in frontal cortex of adult offspring of Poly(I:C)-exposed dams. RESULTS:Exposure to poly(I:C) during gestation impaired probabilistic reversal learning and decreased social approach in MIA offspring compared to controls. We found long-term effects of MIA on expression of 24 genes, including genes involved in glutamatergic neurotransmission, mTOR signaling and potassium ion channel activity. Correlations between gene expression and specific behavioral measures provided insight into genes that may be responsible for ASD-like behavioral alterations. CONCLUSIONS:These findings suggest that MIA can lead to impairments in cognitive flexibility in mice similar to those exhibited in ASD individuals, and that these impairments are associated with altered gene expression in frontal cortex.

| S-EPMC6474674 | biostudies-literature

Maternal immune activation impairs cognitive flexibility and alters transcription in frontal cortex

Project description:Maternal immune activation impairs cognitive flexibility and alters transcription in frontal cortex

| PRJNA565729 | ENA

Frontal Cortex Transcriptome Analysis of Mice Exposed to Electronic Cigarettes During Early Life Stages

Project description:Our study demonstrated that e-cigarettes, both with and without nicotine, induced sex-dependent gene expression change. This RNA-seq study examined the expression profiles of brain frontal cortex samples from mice exposed to classic tobacco flavored bluâ¢ e-cigarettes during gestation and lactation. Brains were extracted and sectioned from ~1-month-old male and female offspring the week following exposure, RNA was isolated and purified from frontal cotrex tissues, and gene expression profiles were analyzed by RNA Sequencing.

2016-02-01 | E-GEOD-75858 | biostudies-arrayexpress

Transcription profiling of response of Rattus norvegicus frontal cortex to chronic olanzapine treatment

Project description:Male Sprague-Dawley albino rats (Charles River) initially weighting approximately 200 grams were randomly assigned to one of the following: 1) olanzapine (2 mg/kg/day, I.P.) (N=20) or 2) Saline (N=20) and administered olanzapine or saline for 21 days. Frontal cortex (N=4/group) was dissected and homogenized for microarray, QPCR and western blotting following previous methods (Fatemi et al. 2003; Brooks et al. 2003). RNA isolation, cDNA preparation, microarray hybridization and QPCR followed previous methods (Brooks et al. 2003).

2007-11-03 | E-GEOD-2547 | biostudies-arrayexpress

Early life sleep disruption alters glutamate and dendritic spines in prefrontal cortex and impairs cognitive flexibility in prairie voles.

Project description:Early life experiences are crucial for proper organization of excitatory synapses within the brain, with outsized effects on late-maturing, experience-dependent regions such as the medial prefrontal cortex (mPFC). Previous work in our lab showed that early life sleep disruption (ELSD) from postnatal days 14-21 in the highly social prairie vole results in long lasting impairments in social behavior. Here, we further hypothesized that ELSD alters glutamatergic synapses in mPFC, thereby affecting cognitive flexibility, an mPFC-dependent behavior. ELSD caused impaired cued fear extinction (indicating cognitive inflexibility), increased dendritic spine density, and decreased glutamate immunogold-labeling in vesicular glutamate transporter 1 (vGLUT1)-labeled presynaptic nerve terminals within mPFC. Our results have profound implications for neurodevelopmental disorders in humans such as autism spectrum disorder that also show poor sleep, impaired social behavior, cognitive inflexibility, as well as altered dendritic spine density and glutamate changes in mPFC, and imply that poor sleep may cause these changes.

| S-EPMC9060254 | biostudies-literature

Parkinson Disease Frontal Cortex ncRNA Profiling

Project description:Parkinson Disease Frontal Cortex ncRNA Profiling

| PRJNA659521 | ENA

Parkinson Disease Frontal Cortex Transcriptomic analysis

Project description:Parkinson Disease Frontal Cortex Transcriptomic analysis

| PRJNA659523 | ENA

Transcriptome Alterations in Myotonic Dystrophy Frontal Cortex

Project description:Transcriptome Alterations in Myotonic Dystrophy Frontal Cortex

| PRJNA661286 | ENA

Effects of Iron Deficiency and Risperidone treatment on the rat frontal cortex

Project description:Prenatal iron deficiency (pID) has been described to increase the risk for neurodevelopmental disorders such as autism and schizophrenia; however, the precise molecular mechanisms are still unknown. Here, we utilized high throughput mass spectrometry to examine the proteomic effects of pID in adulthood on the rat frontal cortex area (FCA). In addition, the FCA proteome was examined in adulthood following risperidone treatment in adolescence to see if these effects could be prevented. We identified 1501 proteins of which 100 were significantly differentially expressed in the FCA at post-natal day 90. Pathway Analysis of proteins affected by pID revealed changes in metabolic processes, including the tricyclic acid cycle, mitochondrial dysfunction, and P13K/Akt signaling. Interestingly, most of these protein changes were not present in the adult pID offspring who received risperidone in adolescence. Behavioral testing of pID rats demonstrated social impairment and poor performance during novelty-induced exploration in pID animals in line with a abnormal neurodevelopmental phenotype. Considering the link between prenatal iron deficiency and several neurodevelopmental disorders such as autism and schizophrenia these presented results bring new perspectives to understand the role of iron in metabolic pathways and provide novel biomarkers for future studies of prenatal iron deficiency.

2018-07-05 | PXD004975 | Pride

Microarrays of frontal cortex (area 8) of Parkinson cases and controls

Project description:Microarrays of frontal cortex (area 8) of Parkinson cases and controls

2013-06-02 | E-MTAB-1194 | biostudies-arrayexpress