Quantitative analysis of hippocampal transcriptomes of naïve and post-status epilepticus (SE) mouse with or without levetiracetam (LEV).
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE205373 | GEO | 2022/06/09
REPOSITORIES: GEO
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Project description:Transient brain insults including status epilepticus (SE) can initiate a process termed ‘epileptogenesis’ that results in chronic temporal lobe epilepsy (TLE). As a consequence, the entire tri-synaptic circuit of the hippocampus is fundamentally impaired. A key role in epileptogenesis has been attributed to the CA1 region as the last relay station in the hippocampal circuit and as site of aberrant plasticity, e.g. mediated by acquired channelopathies. The transcriptional profiles of the distinct hippocampal neurons are highly dynamic during epileptogenesis. Here, we aimed to elucidate the early SE-elicited mRNA signature changes and the respective upstream regulatory cascades in CA1. RNA sequencing of CA1 was performed in the mouse pilocarpine-induced SE model at multiple time points ranging from 6 to 72 hours after the initial insult. Bioinformatics was used to decipher altered gene expression, signalling cascades and their corresponding cell type profiles. Robust transcriptomic changes were detected at 6h after SE and at subsequent time points during early epileptogenesis. Major differentially expressed mRNAs encoded primarily immediate early and excitability-related gene products, as well as genes encoding immune signalling factors.
2023-12-20 | GSE241219 | GEO
Project description:SE was induced in mice (NMRI) chemically by a single dose of Pilocarpine (300mg/kg;i.p.). RNA was extracted from the hippocampi of treated and wild-type mice at 24 h and 28 d after induction. microRNA expressions were measured via microarray technology using Exiqon's miCURY™ LNA Arrays. 4 conditions, Pilocarpine treated mice at 24 h and 28 d, and the control wild-type at the same types, each of 8 replicates.
2014-01-01 | E-GEOD-51841 | biostudies-arrayexpress
Project description:SE was induced in mice (NMRI) chemically by a single dose of Pilocarpine (300mg/kg;i.p.). RNA was extracted from the hippocampi of treated and wild-type mice at 24 h and 28 d after induction. microRNA expressions were measured via microarray technology using Exiqon's miCURY™ LNA Arrays.
2014-01-01 | GSE51841 | GEO
Project description:miRNA array comparing the transcription profile of control rats and rats after intra-hippocampal pilocarpine-induced Status Epilepticus (PILO-SE).
2016-04-28 | E-MTAB-4633 | biostudies-arrayexpress
Project description:We recently developed a fly model of pentylenetetrazol (PTZ)-induced long-term behavioral plasticity. Pharmacological validation suggests this model to be kindling-like. Hence, our model is of relevance in understanding the molecular pathogenesis of epileptogenesis as well as in screening potential antiepileptogenic agents. Levetiracetam (LEV) is considered to have antiepileptogenic activity. Our fly model also predicted similar activity in LEV. Since the mechanism of action of LEV is not clearly known, we have examined the gene expression profiles of fly heads secondary to three days long chronic LEV treatment in Drosophila. Our results provide novel insights in to the drug’s mode of action. Keywords: Drug Response
2007-10-04 | GSE7488 | GEO
Project description:Quantitative analysis of hippocampal transcriptomes of naïve and post-status epilepticus (SE) mouse with or without levetiracetam (LEV).
| PRJNA844899 | ENA
Project description:Status Epilepticus (SE) is an abnormally prolonged seizure that results from either a failure of mechanisms that terminate seizures or from initiating mechanisms that inherently lead to prolonged seizures. Here we report an unbiased analysis of the hippocampal transcriptome of mice with targeted disruption of Dio2 in the astrocytes (Astro-D2KO mouse) undergoing 3 h SE.
2018-05-25 | GSE114887 | GEO
Project description:Status epilepticus (SE) is a life-threatening condition that can give rise to a number of neurological disorders, including learning deficits, depression, and epilepsy. Many of the effects of SE appear to be mediated by alterations in gene expression. To gain deeper insight into how SE affects the transcriptome, we employed the pilocarpine SE model in mice and Illumina-based high-throughput sequencing to characterize alterations in gene expression from the induction of SE, to the development of spontaneous seizure activity. While some genes were upregulated over the entire course of the pathological progression, each of the three sequenced time points (12-hour, 10-days and 6-weeks post-SE) had a largely unique transcriptional profile. Hence, genes that regulate synaptic physiology and transcription were most prominently altered at 12-hours post-SE; at 10-days post-SE, marked changes in metabolic and homeostatic gene expression were detected; at 6-weeks, substantial changes in the expression of cell excitability and morphogenesis genes were detected. At the level of cell signaling, KEGG analysis revealed dynamic changes within the MAPK pathways, as well as in CREB-associated gene expression. Notably, the inducible expression of several noncoding transcripts was also detected. These findings offer potential new insights into the cellular events that shape SE-evoked pathology.
2015-08-27 | GSE72402 | GEO
Project description:Status epilepticus (SE) is a life-threatening condition that can give rise to a number of neurological disorders, including learning deficits, depression, and epilepsy. Many of the effects of SE appear to be mediated by alterations in gene expression. To gain deeper insight into how SE affects the transcriptome, we employed the pilocarpine SE model in mice and Illumina-based high-throughput sequencing to characterize alterations in gene expression from the induction of SE, to the development of spontaneous seizure activity. While some genes were upregulated over the entire course of the pathological progression, each of the three sequenced time points (12-hour, 10-days and 6-weeks post-SE) had a largely unique transcriptional profile. Hence, genes that regulate synaptic physiology and transcription were most prominently altered at 12-hours post-SE; at 10-days post-SE, marked changes in metabolic and homeostatic gene expression were detected; at 6-weeks, substantial changes in the expression of cell excitability and morphogenesis genes were detected. At the level of cell signaling, KEGG analysis revealed dynamic changes within the MAPK pathways, as well as in CREB-associated gene expression. Notably, the inducible expression of several noncoding transcripts was also detected. These findings offer potential new insights into the cellular events that shape SE-evoked pathology. cDNA from two animals was pooled into two independent biological replicates for each timepoint (ie. two sets of two animals per experimental group: control, 12 hours, 10 days, 6 weeks). Samples were sequenced using a Genome Analyzer II (GAII) at a concentration of 10pM in each lane. Base-calling was conducted with the standard Illumina Analysis Pipeline 1.0 (Firescrest-Bustard). Eight FASTQ sequence files (sequencing reads plus quality information) were generated and mapped to the mouse genome (UCSC mm9) using the Bowtie algorithm with default settings. A C++ program was used to count the number of uniquely mapped reads within exons of Ref-Seq genes (UCSC Genome Browser mm9 annotation).
2015-08-27 | E-GEOD-72402 | biostudies-arrayexpress
Project description:Purpose: to evaluate changes in the transcriptome of hippocampal cells during the course of epileptogenesis, from the early events post status epilepticus (SE) to the onset of recurrent spontaneous seizures. Experimental Design: Gene expression profiling was analyzed in hippocampi of rats subjected to the pilocarpine model of epilepsy at different times during the course of epileptogenesis: 3 days post-SE (3D), 7 days post-SE (7D), and immediately (up to 12h) after the first spontaneous seizure (Chronic). All three pilocarpine subgroups had a corresponding age-matched control group (saline-treated rats), from which normal hippocampi samples were obtained at the same experimental time points. Independent microarray hybridizations were carried out for each sample (n = 5, per experimental group) with oligonucleotide microarrays covering 34,000 transcripts representing most of the known and predictive genes of the rat genome (CodeLink⢠Rat Whole Genome Bioarrays, GE Healthcare), following the manufacturerâs protocol. Results: differential expression of almost 1,400 genes was detected during the course of epileptogenesis, from the early events post status epilepticus (SE) to the onset of recurrent spontaneous seizures. Most of these genes are novel and displayed an up-regulation after SE. Noteworthy, a group of 128 genes functioning in neurogenesis, apoptosis, immune response, and intracellular signal transduction was found consistently hyper-expressed throughout epileptogenesis, indicating stable molecular alterations within the hippocampus. Those include modulation of the MAPK, Jak-STAT, PI3K, TGF-beta, and mTOR signaling pathways. Differential expression of genes from the p38 MAPK pathway, mediating inflammation and neurogenesis, was also confirmed by real-time PCR. These findings reveal dynamic molecular changes occurring in the hippocampus that may serve as a starting point for the generation of new hypothesis regarding the underlying mechanisms of epilepsy and for the designing of alternative therapeutic strategies. Keywords: gene expression changes during epileptogenesis. We performed a genome wide analysis of genes differentially expressed during epileptogenesis. Virtually, all possible changes in the rat transcriptome were monitored at distinct time points corresponding to the latent to chronic phase transition of the pilocarpine model of epilepsy, which is probably the most extensively studied chemically inductive model of TLE. Genes identified as being differentially expressed were classified based on their respective biological functions to envisage processes and pathways likely implicated in epileptogenesis, as well as their possible value as targets for therapy. Results were expressed as fold variation, and genes displaying greater than 2-fold changes in transcript abundance and p<0.01 were selected.
2010-02-09 | E-GEOD-14763 | biostudies-arrayexpress