The Genetic Audiogenic Seizure Hamster from Salamanca (GASH/Sal), an animal model of reflex epilepsy, exhibits generalized tonic–clonic seizures in response to loud sound with the epileptogenic focus localized in the inferior colliculus (IC). Ictal events in seizure-prone strains cause gene deregulation in the epileptogenic focus, which can provide insights into the epileptogenic mechanisms. Thus, the present study aimed to determine the expression profile of key genes in the IC of the GASH/Sal after the status epilepticus. For such purpose, we used RNA-Seq to perform a comparative study between the IC transcriptome of GASH/Sal and that of control hamsters both subjected to loud sound stimulation. After filtering for normalization and gene selection, a total of 36 genes were declared differentially expressed from the RNA-seq analysis in the IC. A set of differentially expressed genes were validated by RT-qPCR showing significant differentially expression between GASH/Sal hamsters and Syrian control hamsters. The confirmed differentially expressed genes were classified on ontological categories associated with epileptogenic events similar to those produced by generalized tonic seizures in humans. Subsequently, based on the result of metabolomics, we found the interleukin-4 and 13-signaling, and nucleoside transport as presumably altered routes in the GASH/Sal model. This research suggests that seizures in GASH/Sal hamsters are generated by multiple molecular substrates, which activate biological processes, molecular processes, cellular components and metabolic pathways associated with epileptogenic events similar to those produced by tonic seizures in humans. Therefore, our study supports the use of the GASH/Sal as a valuable animal model for epilepsy research, toward establishing correlations with human epilepsy and searching new biomarkers of epileptogenesis.

中文翻译：

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遗传性听源性癫痫易感仓鼠 GASH/Sal 癫痫持续状态后的下丘转录组

来自 Salamanca 的遗传性听源性癫痫仓鼠 (GASH/Sal)，一种反射性癫痫的动物模型，在响亮的声音下表现出全身强直 - 阵挛性癫痫发作，癫痫病灶位于下丘 (IC)。癫痫发作倾向菌株的发作事件导致致癫痫病灶的基因失调，这可以提供对致癫痫机制的深入了解。因此，本研究旨在确定癫痫持续状态后 GASH/Sal 的 IC 中关键基因的表达谱。为此，我们使用 RNA-Seq 对 GASH/Sal 的 IC 转录组和受到大声刺激的对照仓鼠的 IC 转录组进行了比较研究。在过滤归一化和基因选择后，从 IC 中的 RNA-seq 分析中，共有 36 个基因被宣布为差异表达。一组差异表达的基因通过 RT-qPCR 验证，显示 GASH/Sal 仓鼠和叙利亚对照仓鼠之间的显着差异表达。确认的差异表达基因被分类为与致癫痫事件相关的本体论类别，类似于人类全身性强直发作产生的事件。随后，基于代谢组学的结果，我们发现白细胞介素 4 和 13 信号传导以及核苷转运可能是 GASH/Sal 模型中改变的途径。这项研究表明，GASH/Sal 仓鼠的癫痫发作是由多种分子底物产生的，这些物质会激活与癫痫发作事件相关的生物过程、分子过程、细胞成分和代谢途径，类似于人类强直性癫痫发作产生的那些事件。所以，