耳蜗螺旋神经节的损伤与发育异常将会导致耳聋。神经营养因子在耳蜗螺旋神经节的发育中起重要的作用。我们的前期工作中发现NT3促进螺旋神经节细胞的存活以及神经突起的分化和生长的作用。NT3与其受体TrkC结合后发生生物学效应，但其细胞传递机制尚不明确。研究表明NT3通过MEK/ERK信号通路调控大脑皮层的发育，但MEK/ERK信号通路在耳蜗螺旋神经节发育中的作用方面尚不清楚。本项目拟通过体内实验，检测大鼠耳蜗螺旋神经节组织中TrkC以及下游信号传递因子Ras、MEK、ERK蛋白与mRNA的表达水平；在体内实验中，通过siRNA干扰技术沉默TrkC基因后观察细胞传递的影响，并沉默Ras、MEK、ERK基因后观察其对螺旋神经节细胞发育的影响，从而探讨NT3通过Ras/MEK/ERK信号通路调控大鼠耳蜗螺旋神经节发育的作用机制，为耳聋的预防与早期治疗提供新的靶点。

Damage and developmental abnormalities in the spiral ganglion will result in deafness. Neurotrophic factor plays an important role in the development of spiral ganglion. In our previous study, we found that neurotrophin-3 could promote survival and neurite growth of spiral ganglion neurons. NT3 combined with TrkC has biological effects on the spiral ganglion, but the intracellular signaling pathway is not clear. NT-3 regulates the development of cerebral cortex through MEK/ERK signaling pathway,but the role of MEK/ERK signaling pathway in the development of spiral ganglion is not clear. The purpose of this study is to investigate the expression level of TrkC and downstream signaling factor Ras, MEK, ERK protein and mRNA in rat spiral ganglion tissues in vitro. The influence of cell transmission was observed by siRNA interference technique silencing TrkC gene, and the influence of Ras, MEK and ERK genes on the development of spiral ganglion cells was observed in vivo. To identify the signaling pathway, TrkC、Ras、MEK、ERK were silenced by siRNA, and the survival cells and neurite growth were evaluated. This study in older to certify the mechanism of NT3 through Ras/MEK/ERK signaling pathway to regulate the development of spiral ganglion in rats, and to provide new targets for prevention and early treatment of deafness.