噪声性聋是极为常见的环境因素所致疾病，严重危害着人类的健康。项目组前期研究表明，Ribbon突触易受到噪声暴露的损伤，而且与毛细胞相比，其一旦损伤不易完全修复，因此，Ribbon突触很有可能是噪声暴露所致听觉损伤的主要启动部位；Ribbon突触的损伤是噪声暴露的关键所在，亦是防治噪声损伤的重要突破口。FGF22是FGF家族中的一员，是目前研究的热点之一。现已证实FGF22对促进哺乳动物突触的发育及形成具有重要作用。本项目拟在前期研究及预实验的基础上，验证噪声暴露后豚鼠的听觉生理及Ribbon突触损伤情况；在此基础上探讨携带FGF22的酪氨酸残基变异腺相关病毒耳蜗局部转染拮抗噪声性Ribbon突触损伤，实现噪声性聋防护的可能性。本项目的完成必将推动噪声性聋防治的进一步发展。

Noise-induced hearing loss is a very common disease caused by environmental factors, which seriously harm to human health. Our early experiments confirmed that Ribbon synaptic was susceptible to noise exposure, and uneasy to fully repair once damage comparing with the hair cells. Therefore, Ribbon synapses may be the mainly starting point of auditory injury caused by noise exposure. Ribbon synaptic is the key in damage of noise exposure and  prevention of noise damage. FGF22 is one member of the FGF family, and becoming hot research. It has been proved that FGF22 plays an important role in promoting the development and formation of mammalian synaptic. The purpose of this study was to demonstrate the damage of auditory physiology and Ribbon synaptic  after noise exposure in guinea pigs. On the basis of this tyrosine residue mutation adeno-associated virus carrying FGF22 local transfection of cochlea against the noise Ribbon synaptic damage, it has the possibility of accomplishing the protection of noise induced hearing loss. The completion of the project will further promote the prevention of  noise-induced hearing loss  in future.