Abstract
Temporal lobe epilepsy (TLE) can develop from alterations in hippocampal structure and circuit characteristics, and can be modeled in mice by administration of kainic acid (KA). Adult neurogenesis in the dentate gyrus (DG) contributes to hippocampal functions and has been reported to contribute to the development of TLE. Some of the phenotypical changes include neural stem and precursor cells (NPSC) apoptosis, shortly after their birth, before they produce hippocampal neurons. Here we explored these early phenotypical changes in the DG 3 days after a systemic injection of KA inducing status epilepticus (KA-SE), in mice. We performed a multi-omics experimental setup and analyzed DG tissue samples using proteomics, transcriptomics and microRNA profiling techniques, detecting the expression of 2327 proteins, 13401 mRNAs and 311 microRNAs. We here present a description of how these data were obtained and make them available for further analysis and validation. Our data may help to further identify and characterize molecular mechanisms involved in the alterations induced shortly after KA-SE in the mouse DG.
Highlights
Background & SummaryTemporal lobe epilepsy (TLE) is a serious neuropathological condition hallmarked by chronic spontaneous recurrent seizures, which can originate from altered hippocampal circuit characteristics
TLE is a serious neuropathological condition hallmarked by chronic spontaneous recurrent seizures, which can originate from altered hippocampal circuit characteristics
Concerning aberrant neurogenesis, multiple cellular phenotypes have been linked to the nature of newly born aberrant neurons including alterations in levels of NSPC proliferation, and subsequent changes in the levels of apoptosis, differentiation, integration and ectopic positioning of their progeny[4,5,6]
Summary
TLE is a serious neuropathological condition hallmarked by chronic spontaneous recurrent seizures, which can originate from altered hippocampal circuit characteristics. The current view on TLE development, proposes a number of causal changes in hippocampal structure including DG granule cell layer dispersion[2], mossy fiber sprouting[3], and the induction of aberrant hippocampal neurogenesis[4,5]. These abnormalities can be modeled using convulsant treatments such as e.g., KA administration[4]. A number of previous studies have applied -omics approaches to describe changes in DG gene expression (shortly) after KA-SE at the level of mRNA8. The dataset described here may allow the identification and further characterization of molecular mechanisms that could help to understand the numerous phenotypical alterations taking place in the DG shortly after KA-SE
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