Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-6614
PROVIDER: PRJNA98881 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcription profiling of mouse brains following nicotine-induced seizures
2015-10-13 | E-GEOD-6614 | ExpressionAtlas
Project description:Nicotine, acting through the neuronal nicotinic acetylcholine receptors (nAChR), can induce seizures in mice. We aimed to study brain transcriptional response to seizure and to identify genes whose expression is altered after nicotine-induced seizures. Whole brains of untreated mice were compared to brains one hour after seizure activity, using Affymetrix U74Av2 microaarays. Experimental groups included wild-type mice and both nicotine-induced seizures sensitive and resistant nAChR mutant mice. Each genotype group received different nicotine doses to generate seizures. This approach allowed the identification of significantly changed genes whose expression was dependent on seizure activity, nicotine administration or both, but not on the type of nAChR subunit mutation or the amount of nicotine injected. Significant expression changes were detected in 62 genes (p < 0.05, FDR correction). Among them, GO functional annotation analysis determined that the most significantly over-represented categories were of genes encoding MAP kinase phosphatases, regulators of transcription and nucleosome assembly proteins. In-silico bioinformatic analysis of the promoter regions of the 62 changed genes detected the significant enrichments of 16 transcription regulatory elements (TREs), creating a network of transcriptional regulatory responses to seizures. The TREs for ATF and SRF were most significantly enriched, supporting their association with seizure activity. Our data suggest that nicotine-induced seizure in mice is a useful model to study seizure activity and its global brain transcriptional response. The differentially expressed genes detected here can help understand the molecular mechanisms underlying seizures in animal models, and may also serve as candidate genes to study epilepsy in humans. Experiment Overall Design: Whole brain expression profiles were determined in two experimental groups of mice, sixteen mice that were not treated with nicotine and twelve mice one hour after experiencing nicotine-induced seizure. The untreated group included six wild-type mice, five alpha7+/T and five beta4-/- mice. The group of mice that underwent nicotine-induced seizures included three wild-types, five alpha7+/T and four beta4-/- mice. Different doses of nicotine were injected intraperitoneally (i.p.) to each genotype group of mice in order to achieve a similar seizure score in all three genotypes.
2008-04-09 | E-GEOD-6614 | biostudies-arrayexpress
Project description:Nicotine, acting through the neuronal nicotinic acetylcholine receptors (nAChR), can induce seizures in mice. We aimed to study brain transcriptional response to seizure and to identify genes whose expression is altered after nicotine-induced seizures. Whole brains of untreated mice were compared to brains one hour after seizure activity, using Affymetrix U74Av2 microaarays. Experimental groups included wild-type mice and both nicotine-induced seizures sensitive and resistant nAChR mutant mice. Each genotype group received different nicotine doses to generate seizures. This approach allowed the identification of significantly changed genes whose expression was dependent on seizure activity, nicotine administration or both, but not on the type of nAChR subunit mutation or the amount of nicotine injected. Significant expression changes were detected in 62 genes (p < 0.05, FDR correction). Among them, GO functional annotation analysis determined that the most significantly over-represented categories were of genes encoding MAP kinase phosphatases, regulators of transcription and nucleosome assembly proteins. In-silico bioinformatic analysis of the promoter regions of the 62 changed genes detected the significant enrichments of 16 transcription regulatory elements (TREs), creating a network of transcriptional regulatory responses to seizures. The TREs for ATF and SRF were most significantly enriched, supporting their association with seizure activity. Our data suggest that nicotine-induced seizure in mice is a useful model to study seizure activity and its global brain transcriptional response. The differentially expressed genes detected here can help understand the molecular mechanisms underlying seizures in animal models, and may also serve as candidate genes to study epilepsy in humans. Keywords: treatment, seizure activity, genotypes
2007-12-26 | GSE6614 | GEO
Project description:To examine irreversible changes in the developing brain following seizures, juvenile inbred mice were intraperitoneally injected with kainate and nicotine. Keywords: seizure induction
2007-01-04 | GSE6388 | GEO
Project description:To examine irreversible changes in the developing brain following seizures, juvenile inbred mice were intraperitoneally injected with kainate and nicotine. Experiment Overall Design: Kainate and nicotine were dissolved in sterile saline, and intraperitoneally injected into postnatal day 23 males at a dose of 15 mg/kg and 10 mg/kg, respectively. Control mice received a comparable injection of saline. The injection was repeated three times at 2-hour intervals in the daytime, and after one week, the P30 survivors were sacrificed for sample preparation. Neocortices and hippocampi were isolated from mice that had received the repeated injections of saline, kainate, and nicotine (n=6, 5, and 6 mice, respectively).
2008-06-14 | E-GEOD-6388 | biostudies-arrayexpress
Project description:Transcription profiling of hippocampus from wild type and ZIF268(Egr1) knock-out mice subjected to kainic acid induced seizures
2015-10-22 | E-MEXP-1483 | ExpressionAtlas
Project description:Hepatic gene expression changes following antisense oligonucleotide-based inhibition of miR-29a
2015-09-30 | E-GEOD-40261 | ExpressionAtlas
Project description:This study aims to investigate age-specific, time-dependent changes in gene expression that may underlie the priming effect of early-life seizures by looking at the sequence of gene expression patterns in the hippocampus at various times following Kainate induced seizures at postnatal day (P) 15. Keywords: other
2004-03-29 | GSE1156 | GEO
Project description:Developmental nicotine exposure causes persistent changes in cortical neuron morphology and in behavior. We used microarray screening to identify master transcriptional or epigenetic regulators mediating these effects of nicotine and discovered increases in Ash2l, a component of a histone methyltransferase complex. We therefore examined genome-wide changes in H3MeK4 tri-methylation, a mark induced by the Ash2l complex associated with increased gene transcription. A significant number of regulated promoter sites were involved in synapse maintenance. We found that Mef2c interacts with Ash2l and mediates changes in H3MeK4 trimethylation. Knockdown of Ash2l or Mef2c abolishes nicotine-mediated alterations of dendritic complexity in vitro and in vivo, and attenuates nicotine-dependent changes in passive avoidance behavior. In contrast, overexpression mimics nicotine-mediated alterations of neuronal structure and passive avoidance behavior. These studies identify Ash2l as a novel target induced by nicotinic stimulation that couples developmental nicotine exposure to changes in brain epigenetic marks, neuronal structure and behavior.
2016-05-30 | GSE80788 | GEO
Project description:This study aims to investigate age-specific, time-dependent changes in gene expression that may underlie the priming effect of early-life seizures by looking at the sequence of gene expression patterns in the hippocampus at various times following Kainate induced seizures at postnatal day (P) 15.
2007-10-27 | E-GEOD-1156 | biostudies-arrayexpress