感音神经性聋是最常见的听觉残疾，内耳毛细胞的突触病变是其发生的重要病理机制。研究表明Otoferlin基因在成熟内耳毛细胞特异性高度表达，是维持突触囊泡胞吐释放递质的关键蛋白，但其调控机制并不清楚。我们前期实验结果提示Otoferlin在维持听力的过程中起重要作用，结合前期miRNA芯片获得的信息以及生物信息学分析结果，推测miR-486-5p可能对Otoferlin基因表达起调控作用。因此本项目拟结合突触电生理、激光共聚焦检测电磁辐射辐照前后小鼠miR-486-5p的表达，运用蛋白印迹、FISH和形态学检测相结合的方法鉴定Otoferlin为该miRNA的靶基因，通过对囊泡递质谷氨酸的检测明确miR-486-5p调控Otoferlin表达的因果关系，解析其在突触囊泡递质释放过程中的调控功能。通过研究，初步明确突触囊泡调控信号通路的可能蛋白位点，最终为听功能损伤的防护提供实验依据。

sensorineural deafness is the most common hearing disability,and the synaptic pathobiology of inner ear is important.Some researches showed that Otoferlin gene specifically express high level in mature inner ear,which is the key protein used to maintenance the exocytosis of synaptic vesicles,but its regulation mechanism is unknown.Our initial studies suggested that Otoferlin plays an important role in maintaining hearing,according to initial information getting from the miRNA chip and the analysis by bioinformatics,we suppose that miR-486-5p may regulate the expression of Otoferlin gene.Then we plan to perform a project that combine with electrophysiology,confocal laser detection electromagnetic radiation before and after irradiation mice miR-486-5 p expression,western blotting,FISH and morphologic detection method to demonstrate whether Otoferlin is target gene of miRNA.According to the study, preliminary confirm possible protein sites in signaling pathways underlying the control by synaptic vesicles,and provide foundation to the protection for the hearing loss.