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Commonalities in gene expression and methylation changes across two rat models of acquired epilepsy [RRBS]

ABSTRACT: Epileptogenesis, the process by which a normal brain develops epilepsy, is characterized by complex changes in DNA methylation and gene expression. In this study, RNA sequencing and reduced-representation bisulfite sequencing were utilized to investigate these molecular alterations in two distinct and widely used rat models of temporal lobe epilepsy: intrahippocampal electrical kindling and systemic kainic acid. These models, involving rats, differ significantly in their underlying mechanisms and histopathological outcomes, providing a unique opportunity to identify both shared and model-specific changes during epileptogenesis. By comparing these models, we uncovered common pathways that may reflect generalizable, model-independent mechanisms of epileptogenesis, alongside distinct changes that highlight the diverse molecular landscapes of each model. This integrative, multi-omics approach not only enhances our understanding of the molecular drivers of epileptogenesis but also underscores the importance of cross-model comparisons for uncovering robust and potentially therapeutic targets in epilepsy research. This dataset serves as a valuable resource for exploring the epigenomic and transcriptomic underpinnings of epilepsy.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE287822 | GEO | 2026/01/23

REPOSITORIES: GEO

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Commonalities in gene expression and methylation changes across two rat models of acquired epilepsy [RNA-seq]

Project description:Epileptogenesis, the process by which a normal brain develops epilepsy, is characterized by complex changes in DNA methylation and gene expression. In this study, RNA sequencing and reduced-representation bisulfite sequencing were utilized to investigate these molecular alterations in two distinct and widely used rat models of temporal lobe epilepsy: intrahippocampal electrical kindling and systemic kainic acid. These models, involving rats, differ significantly in their underlying mechanisms and histopathological outcomes, providing a unique opportunity to identify both shared and model-specific changes during epileptogenesis. By comparing these models, we uncovered common pathways that may reflect generalizable, model-independent mechanisms of epileptogenesis, alongside distinct changes that highlight the diverse molecular landscapes of each model. This integrative, multi-omics approach not only enhances our understanding of the molecular drivers of epileptogenesis but also underscores the importance of cross-model comparisons for uncovering robust and potentially therapeutic targets in epilepsy research. This dataset serves as a valuable resource for exploring the epigenomic and transcriptomic underpinnings of epilepsy.

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Transcriptional profiling of dentate granule cells in 4 rat epilepsy models

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Project description:Mesial Temporal Lobe Epilepsy is characterized by progressive changes of both neurons and glia, also referred to as epileptogenesis. No curative treatment options, apart from surgery, are available. DNA methylation (DNAm) is a potential upstream mechanism in epileptogenesis and may serve as a novel therapeutic target. To our knowledge, this is the first study to investigate epilepsy-related DNAm, gene expression (GE) and their relationship, in neurons and glia. We used the intracortical kainic acid injection model to elicit status epilepticus. At 24 hours post injection, hippocampi from eight kainic acid- (KA) and eight saline-injected (SH) mice were extracted and shock frozen. Separation into neurons and glial nuclei was performed by flow cytometry. Changes in DNAm and gene expression were measured with reduced representation bisulfite sequencing (RRBS) and mRNA-sequencing (mRNAseq). Statistical analyses were performed in R with the edgeR package. We observed fulminant DNAm- and GE changes in both neurons and glia at 24 hours after initiation of status epilepticus. The vast majority of these changes were specific for either neurons or glia. At several epilepsy-related genes, like HDAC11, SPP1, GAL, DRD1 and SV2C, significant differential methylation and differential gene expression coincided. We found neuron- and glia-specific changes in DNAm and gene expression in early epileptogenesis. We detected single genetic loci in several epilepsy-related genes, where DNAm and GE changes coincide, worth further investigation. Further, our results may serve as an information source for neuronal and glial alterations in both DNAm and GE in early epileptogenesis.

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