贵州省万山汞矿区长期的开采冶炼活动对当地土壤、大气和水体造成了严重的污染，当地居民存在较高的甲基汞暴露风险。动物实验和流行病学资料都已证实，妊娠期和哺乳期甲基汞暴露可造成子代学习记忆损伤、认知障碍、语言障碍等脑损伤，但其机制不明是制约临床早期诊断、早期治疗的瓶颈。本课题以海马神经元VGCC、LTP电生理特性为研究靶点，利用全细胞膜片钳结合动物行为学实验、Real-time PCR、Western-Blot、免疫组化、细胞转染等技术，探讨miR-9和FoxP2在甲基汞致子代学习记忆损伤中的作用机制。在此基础上构建过表达和抑制模型，进一步论证miR-9和FoxP2靶向调控关系在海马神经元损伤中的作用，以期为甲基汞暴露造成子代神经毒性的早诊断、早治疗提供新的靶标和思路。

Long-term mining and smelting activities in the Wanshan mercury mine area of Guizhou province have caused serious pollution to the local soil, atmosphere and water bodies, resulting in a higher risk of exposure to methylmercury in the local population. Exposure to methylmercury in pregnancy and lactation periods may induce brain injuries of filial generation, such as learning-memory dysfunction, cognitive disorder and language barrier which have confirmed by animal experiments and epidemiological studies. However, its mechanism is unknown, which is the bottleneck of early diagnosis and treatment. In order to investigate the possible mechanism of miR-9 and FoxP2 in learning-memory impairment induced by methylmercury, we use whole cell patch clamp technique combined with animal behavior experiment, Real-time PCR，Western-Blot，immunohistochemistry and cell transfection techniques, and the electrophysiological characteristic of VGCC and LTP in hippocampal neurons is our stduy target. The current study aims to further demonstrate the targeted regulation relationship of miR-9 and FoxP2 in hippocampal neuron damage through gain and loss-of-function approaches and provide novel therapeutic targets and strategies for early diagnosis and early treatment.