噪声性聋是极为常见的环境因素所致疾病，严重危害人类的健康。我们的前期研究发现，低强度噪声暴露后Ribbon突触的损伤是听力下降的原因；伴随其大量修复，听力亦恢复正常。进一步地研究发现，突触修复后尽管听力阈值恢复正常，但耳蜗复合动作电位仅有轻微恢复，提示听觉功能仍存在障碍。囊泡快速、精确地释放神经递质是Ribbon突触功能正常的关键环节。囊泡谷氨酸转运体3（vesicular glutamate transporter3，VGLUT3）是影响谷氨酸能突触传递的主要蛋白，与耳聋的发生密切相关。预实验发现VGLUT3表达下降，提示VGLUT3降低可能是低强度噪声暴露后听觉功能障碍的原因。本项目拟在前期研究的基础上，确证低强度噪声暴露后，VGLUT3在毛细胞的表达的水平和Ribbon突触囊泡的数量的变化，以及这种变化与听功能障碍的关系；并在此基础上探讨改善低强度噪声导致听觉功能障碍的可行性及机制。

Noise induced hearing loss is extremely common diseases caused by environmental factors, seriously endangering human health. We found that Ribbon synaptic damage is the cause of hearing loss after low intensity noise exposure; with the large repair, normal hearing restores. Further study found that although the synapse repaired, after hearing thresholds returned to normal, only a slight recovery of cochlear compound action potentials, which suggesting that there are still obstacles to auditory function. Vesicular neurotransmitter quick and accurate releasement is the key to the normal Ribbon synaptic function. Vesicular glutamate transporter 3 (VGLUT3) is the main protein that influence glutamatergic synaptic transmission, and is closely related to the occurrence of deafness. The previous experiment found that the expression of VGLUT3 decreased, suggesting that the decrease expression of VGLUT3 may be a cause of hearing dysfunction after exposure to noise. Therefore, this project aims on the basis of previous research, to confirm after low intensity noise exposure, the change of expression level of VGLUT3 vesicles in the hair cells and the ribbon synaptic vesicle number, and the relationship between this change and hearing impairment; the feasibility and mechanisms of antagonism of hearing dysfunction leaded by low intensity noise.