保护和治疗受损的螺旋神经节细胞（SGN）对预防和治疗听力下降有重大意义。我们前期发现发育阶段的SGN较成熟SGN更易受耳毒性药物损害。文献表明TRPC3通道蛋白可以非选择性地透过庆大霉素等多种阳离子，在发育期SGN神经纤维上短暂高表达，并可促进受损成熟神经元的存活。提示TRPC3与SGN的发育、发育中的药物损伤及损伤后的保护有关。因此本研究拟了解TRPC3在CBA/J小鼠发育期SGN及受损的成熟SGN上的表达变化；探索它与卡那霉素及重金属的神经毒性的关系；用磷酸化抗体芯片筛选TRPC3在钙离子通道中的下游分子，阐明其在SGN发育中的作用机制；再反向调节TRPC3和其下游分子，探索既能抑制TRPC3所介导的药物性损伤又不影响神经元发育的SGN保护方案；最后探索TRPC3对保护受损的成年SGNs的作用。以期为保护发育阶段的SGN、治疗听力损伤提供新的靶点和思路。

It is of great importance to protect the spiral ganglion neurons (SGN) and to prevent their damage in treating and preventing hearing loss. We found out in our previous studies that the developing SGNs are more vulnerable to ototoxic materials than their mature counterparts. Many literatures reported that the canonical transient receptor potential 3 (TRPC3) can non-selectively transport various positive ions and is temporarily highly expressed at the terminals of the SGNs' fibers and related to the survival of impaired mature neurons. These literatures suggest that TRPC3 is related to the development and the neurotoxic susceptibility of the juvenile SGNs and the protection of the impaired mature ones. In this study, we are going to elucidate the expression pattern of TRPC3 in the developing SGNs and their impaired mature counterparts of CBA/J mice; to explore its role in facilitating the neurotoxicity of kanamycin and heavy metal ions, and to delve its effects upon the SGNs' development and its downstream effectors in the calcium ion pathway by applying a phosphorylated antibody chip. Then we will go further to manipulate the functions of TRPC3 and its effectors in opposite directions to explore whether we can suppress the TRPC3 facilitated neurotoxic susceptibility without interfering the development of SGNs. And finally we will explore the effects of TRPC3 on the protection of the impaired mature SGNs. All together, we hope our study can shed a new light on the protection of the developing SGNs and the treatment of hearing loss.