双极细胞是光遗传学治疗视网膜变性疾病最理想的靶细胞，视网膜变性晚期双极细胞伸出异常突起严重阻碍其临床应用，因此探索双极细胞异常突起形成的机制并进行干预有重要意义。课题组预实验发现RCS大鼠变性晚期视杆双极细胞（RBs）伸出异常突起，表达mGluR6下降，可能表达AMPA受体。结合文献AMPA受体GluR2在其他视网膜变性动物RBs表达增加，以及GluR2在中枢神经系统的功能，我们推测视网膜变性过程中RBs上调GluR2表达促进异常突起形成。本课题拟从以下方面进行研究：⑴明确视网膜变性过程中GluR2与RBs异常突起的相关性；⑵在体实验下调RCS大鼠、上调正常大鼠GluR2表达观察对RBs突起生长的影响；⑶离体实验上调RBs中GluR2表达观察对突起生长的影响并初步探索其分子机制。本研究有助于明确视网膜变性中RBs异常突起形成的机制，为进一步探索抑制双极细胞异常突起形成的方法提供理论基础。

Bipolar cells are the ideal target cells of optogentic therapy for retinal degeneration (RD). Neuritogenesis of bipolar cells in late RD compromises optogentic therapy. Thus elucidating the mechanism of neuritogenesis of bipolar cells is impending. Our previous studies showed that rod bipolars (RBs) sprouted anomalous neuritogenesis in late RD in RCS rats. At the same time, mGluR6 was down regulated and AMPA was upregulated. Literature review revealed that GluR2 subunit of AMPA was upregulated in other RD models. And in the central nervous system, GluR2 play critical roles in the regulation of neurite outgrowth. We hypothesized that GluR2 upregulation promote anomalous neuritogenesis of RBs. In the present study, the correlation between GluR2 expression and anomalous neuritogenesis in RCS rats will be studied. Then GluR2 was up and downregulated in RCS and normal rats to study its role in dendrite growth of RBs in vivo. At last GluR2 was upreglated in primarily cultured retinal cells to further study its role in dendrite growth of RBs in vitro and the potential mechanism. The present study might help in elucidating the mechanisms underlying neuritogenesis of bipolar cells, and provide theoretical basis for exploring ways to inhibit neuritogenesis.