耳鸣发病率高，但发病机制未明，其中，谷氨酸（Glu）的改变可引起耳鸣，囊泡谷氨酸转运体3（VGLUT3）控制耳蜗谷氨酸释放，敲除 VGLUT3基因，小鼠听力丧失。并且，VGLUT3 同时存在于兴奋性神经元及抑制性神经元中，其改变可导致抑制性神经元功能失调，引起兴奋/抑制失衡。我们前期研究发现：水杨酸钠作用后，耳蜗螺旋神经节细胞VGLUT3表达量增强，Glu表达升高，GABA表达降低。据而推测：VGLUT3表达的改变可能是引起耳鸣的机制之一。 因此，本实验拟采用水杨酸钠诱导大鼠耳鸣，听觉惊跳反射前抑制实验进行模型检测，辅助免疫组化﹑分子生物学﹑形态学及电生理等技术，检测⑴耳蜗及下丘核VGLUT3表达量、分布改变；⑵毛细胞突触及下丘核神经突触的形态学及VGLUT3超微表达的改变；⑶应用VGLUT3抑制剂后上述指标的变化，从而探讨VGLUT3在水杨酸钠致耳鸣中的作用。

The pathogenesis of tinnitus is still unknown. The excitement / inhibition balance disorders account for an important role in the neural mechanisms of tinnitus generated. Vesicular glutamate transporter 3 (VGLUT3) is related to the release of glutamate in the cochlea, the knockout mice of VGLUT3 is completely hearing loss. Moreover, VGLUT3 is glutamatergic neuron-specific marker, but coexist in the inhibitory neurons, which may lead to changes in inhibitory neuronal function disorders, thereby causing excitement / inhibition imbalance. In addition, our previous study found: salicylate could made the over expression of VGLUT3 in the rat spiral ganglion cells. It suggested: changes of VGLUT3 may be one of the mechanisms causing neuronal excitement / inhibition imbalance. Therefore , the present study intends to use salicylate to induce tinnitus , using auditory startle reflex inhibition to text the model, assisted with immunohistochemistry, molecular biology, morphological and electrophysiological techniques to detect the ⑴ changes of the number and distribution of VGLUT3in the cochlea and inferior colliculus ;⑵ changes of morphology and expression of ultrafine VGLUT3 in the synapse of inner hair cells and inferior colliculus synapse;⑶ a specific inhibitor administered would be used to evaluate the degree of damage caused by tinnitus, with an expectation to uncover the major principle of salicylate-induced tinnitus.