本项目利用已建立的大鼠内侧颞叶癫痫（MTLE）动物模型、体外培养神经元癫痫细胞模型，结合质粒转染、膜片钳、RT-qPCR、免疫印迹、激光扫描共聚焦等研究策略，开创性的研究microRNA、炎症反应和突触可塑性在MTLE慢性化进程中的作用及机制。本研究首次提出在MTLE形成的极早期，各种刺激因素(惊厥、感染、缺血、外伤等)导致星形胶质细胞上TLR4表达上调，炎症相关性microRNA通过调控TLR4/NF-κB信号通路及炎症因子的表达，参与炎症反应的启动。随后海马内的慢性炎症促使神经元表达脑源性神经生长因子增加，通过磷酸化ERK/CREB途径影响突触的形态及功能，促进MTLE的慢性化进程，而突触相关性microRNAs参与了这个过程的调控。对此问题的深入探讨，对阐明MTLE慢性化进程的发生、发展具有里程碑式的意义，并为MTLE的早期防治提供了一个全新的思路。

The influence and mechanism of microRNA expression, inflammatory response and synaptic plasticity in the mesial temporal lobe epilepsy (MTLE) pathogenesis were explored by means of plasmic transfection, patch-clamp, RT-qPCR, immunoblotting and confocal microscopy in established MTLE rat model as well as neuron cultures. We report for the first time that inflammation related microRNAs may contribute to trigger inflammatory and innate immune response by modulate inflammatory TLR4/NF-κB/IL-1β signaling pathway in the early stage of MTLE pathogenesis. Consequently, the expression of BDNF significantly increased in hippocampus, which plays critical role in regulation of synaptic plasticity via ERK/CREB phosphorylation, while synaptic related microRNAs may participated in this process. Further investigation may fulfill the task of understanding the mechanism of MTLE development and may allow detecting a potential prophylaxis and treatment target to MTLE.