大量研究表明酸敏感通道ASICla主要表达于中枢抑制性中间神经元，并且与癫痫密切相关，但其在癫痫发生发展过程中的具体细胞分子机制尚不清楚。本课题利用条件性基因敲除PV-ASIC1a-/-小鼠制备颞叶癫痫模型，通过脑电、tetrode多通道电极和全细胞膜片钳技术，从在体（in vivo）和体外（in vitro）两个方面观察PV抑制性中间神经元放电特征，同时从细胞、蛋白等水平观察癫痫发生发展不同阶段ASICla的表达变化；通过上述结果在癫痫患者癫痫灶组织标本中进行印证，以明确ASICla是否通过激活PV阳性中间神经元来调控癫痫发作，从而揭示PV阳性中间神经元上的ASICla参与癫痫的分子机制，为进一步研发ASIC1a为靶点的治疗癫痫药物开拓新的视角。

Many researches showed that acid-sensing ion channel (ASIC1a) is mainly expressed in inhibitory interneurons of CNS, and is closely associated with the occurrence of epilepsy. However, the exact cellular and molecular mechanism remains unclear. In herein study, we observe discharging characteristics changes of PV-positive inhibitory interneurons in vivo and vitro on the PV cre-ASIC1a-/-mice temporal epilepsy model, by using EEG, tetrode multi-channel electrode technology and patch clamp recording technique. The expression changes of ASIC1a at the different stages of epilepsy will be explored at cellular and protein levels. Human temporal epileptogenic focus samples will be also studied to verify the results above. This project aims to explore whether ASIC1a regulate the epileptic seizure through mediating the activation of PV-positive inhibitory interneurons and elucidate the molecular mechanism that ASIC1a might develop in the occurrence of epilepsy. In addition, this research will also provide a new insight to develop antiepileptic medicines targeting on acid-sensing channel in treatment of epilepsy.