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Transcriptomic profiling of the intra-amygdala kainate mouse model across the stages of epileptogenesis

ABSTRACT: Mesial temporal lobe epilepsy (MTLE) is a prevalent form of drug-resistant epilepsy often associated with hippocampal sclerosis (HS). While various rodent models exist to study this condition, their molecular fidelity to human MTLE requires detailed evaluation. As part of a larger cross-species transcriptomic meta-analysis, we generated this dataset to characterize the intra-amygdala kainate mouse model, which provides a unique framework for studying status epilepticus-induced epileptogenesis. We performed bulk RNA-sequencing on hippocampal tissues to capture the evolving molecular landscape during the acute, intermediate, and chronic phases following seizure induction. This dataset allows for the investigation of key epileptogenic processes, including neuroinflammation, neuronal death, and reactive gliosis, and serves as a critical component in comparing chemical induction models against human MTLE pathophysiology.

ORGANISM(S): Mus musculus

PROVIDER: GSE319769 | GEO | 2026/04/16

REPOSITORIES: GEO

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Project description:Morphological changes in mesial Temporal Lobe Epilepsy with Hippocampal Sclerosis (mTLE-HS) are well characterized. Yet it remains elusive whether these are a consequence of seizures or originate from a hitherto unknown underlying pathology. We recently published data on changes in gene expression (GE) and DNA methylation (DNAm) in the ipsilateral hippocampus (ILH), using the intracortical kainate mouse model of mTLE-HS. In order to explore the effects of epileptic activity alone and also to further disentangle what triggers morphological alterations, we investigated glial and neuronal changes in GE and DNAm in the contralateral hippocampus (CLH). The intracortical kainic acid mouse model of mTLE-HS was used to elicit status epilepticus. Hippocampi contralateral to injection site from 8 kainate injected (KA) and 8 sham (SH) mice were extracted, and shock frozen at 24 hours post injection. Glial- and neuronal nuclei were sorted by flow cytometry. Alterations in GE and DNAm were assessed using reduced representation bisulfite sequencing (RRBS) and RNA sequencing (RNAseq). The R package edgeR was used for statistical analysis. The CLH featured substantial, mostly cell-specific changes in both GE and DNAm in glia and neurons. While changes in GE overlapped to a great degree between CLH and ILH, alterations in DNAm did not. In the CLH we found a significantly lower number of glial genes up- and downregulated compared to previous results from the ILH. Furthermore, several genes and pathways potentially involved in anti-epileptogenic effects were upregulated in the CLH. By comparing GE data from the CLH to previous results from the ILH (featuring hippocampal sclerosis), we derive potential upstream targets for epileptogenesis, including glial Cox2 and Cxcl10. Despite the absence of morphological changes, the CLH displays substantial changes in GE and DNAm. We find that GE changes related to potential anti-epileptogenic effects seem to dominate compared to pro-epileptogenic effects in the CLH and speculate whether this imbalance contributes to prevent morphological alterations like neuronal death and reactive gliosis.

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Transcriptomic profiling of the intra-amygdala kainate mouse model across the stages of epileptogenesis

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