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Identification of differentially expressed genes in the hippocampus in the intraamygdala kainic acid mouse model of status epilepticus.

ABSTRACT: The aim of this work was to identify mRNA expression changes in the ipsilateral hippocampus in the intraamygdala kainic acid (KA) mouse model of status epilepticus. In this model, status epilepticus (prolonged damaging seizures) are triggered by an intraamygdala KA injection. All mice develop epilepsy after a short latency period of 3-5 days. For our experiments, 10-week old mice with a C57BL/6 background were either injected with intraamygdala KA (n = 18) or vehicle (PBS, n = 18). Mice were sacrificed 8 hours following status epilepticus (acute pathology) or 14 days post-status epilepticus (timepoint at which all mice suffer from chronic epilepsy) and ipsilateral hippocampi were quickly dissected and pooled into 3 groups (n = 3 per pooled sample).

ORGANISM(S): Mus musculus

PROVIDER: GSE122228 | GEO | 2021/09/09

REPOSITORIES: GEO

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Project description:In this study we used microarray analysis to reveal the gene expression profile of the hippocampal CA1 subregion, which was laser-capture microdissected one week after kainic acid (KA)-induced status epilepticus (SE) in postnatal day 21 (P21) rats. These rats are developmentally roughly comparable to juvenile children, and KA-induced SE leads to selective damage of hippocampal CA1 pyramidal neurons in this age group while saving neurons of the other sub-regions. We searched for alterations in the gene expression pattern during the early epileptogenetic phase, i.e. one week after SE, and compared the results with those of age-matched control rats. To detect specifically changes in the CA1 pyramidal neurons, we used the laser-capture microdissection technique that allows the precise isolation of the region of interest. The RNA of this region was isolated, amplified, and labeled, and then hybridized to Illumina RatRef-12 Expression BeadChip Arrays. The gene expression data generated from the microarray was first normalized by the guantile normalization method, and then filtered by using the empirical Bayes method, and the contrasts were created by using the Limma R/Bioconductor. Finally, the data was clustered by using the non-hierarchical K-means clustering for genes, and the pathway analysis was performed by âGene set testâ, which analyzes the statistical significance of a set of genes simultaneously ranked by p-value and generates the KEGG categories (Chipster manual). The Illumina microarray analysis with the Chipster software v1.1.0 (http://chipster.csc.fi; CSC, Espoo, Finland) generated a total of 1592 differently expressed genes in the CA1 subregion of KA-treated rats compared to control rats. Using the K-means method the genes were classified in 10 different clusters. The subsequent KEGG-test for the probe set over-representation analysis revealed the 15 significantly (p<0.05) changed KEGG-pathways in response to KA-treatment, e.g. oxidative phosphorylation (26 genes changed), and long-term potentiation (LTP; 18 genes changed). Some of the differentially expressed genes were also identified to be involved in Ca2+ homeostasis, gliosis, inflammation, and GABAergic transmission.

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Identification of differentially expressed genes in the hippocampus in the intraamygdala kainic acid mouse model of status epilepticus.

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