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

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.癫痫发生（epileptogenesis）指正常大脑发展为癫痫的病理过程，其特征为DNA甲基化与基因表达的复杂改变。本研究采用RNA测序（RNA sequencing）与简化代表性亚硫酸氢盐测序（reduced-representation bisulfite sequencing），对两种经典且广泛应用的颞叶癫痫大鼠模型中的分子改变进行探究：海马内电点燃模型与全身海人酸（kainic acid）模型。这两种大鼠模型在潜在分子机制与组织病理学结局上存在显著差异，为甄别癫痫发生过程中共享的与模型特异性的分子变化提供了独特契机。通过对这两种模型进行比较，本研究揭示了可反映癫痫发生通用、非模型依赖机制的共通通路，同时也发现了凸显各模型独特分子特征的差异性变化。这种整合式多组学研究方法，不仅加深了我们对癫痫发生分子驱动因素的认知，同时也凸显了跨模型比较在癫痫研究中发掘可靠潜在治疗靶点的重要性。本数据集可为探索癫痫的表观基因组与转录组基础提供宝贵的研究资源。