Selective loss of cone function in mice lacking the cyclic nucleotide-gated channel CNG3
Selective loss of cone function in mice lacking the cyclic nucleotide-gated channel CNG3
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DOI：
10.1073/pnas.96.13.7553
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发表时间：
1999-06-22
影响因子：
11.1
通讯作者：
Hofmann, F
中科院分区：
文献类型：
--
作者：
Biel, M;Seeliger, M;Hofmann, F
两种类型的光感受器，杆和锥，共存于脊椎动物的视网膜。深入分析传递视杆细胞和视锥细胞信号的视网膜回路一直受到视杆细胞和视锥细胞通路之间存在密切的物理和功能联系的阻碍。通过删除环核苷酸门控通道CNG3，我们产生了一个缺乏任何锥介导的光反应的小鼠。相反，在CNG3缺陷小鼠中，视杆细胞通路是完全完整的。视锥功能的功能丧失与视锥光感受器的进行性变性相关，但与其他视网膜细胞类型无关。CNG3缺陷型小鼠提供了明确剖析视杆细胞和视锥细胞通路对正常视网膜功能的贡献的动物模型。
Two types of photoreceptors, rods and cones, coexist in the vertebrate retina. An in-depth analysis of the retinal circuitry that transmits rod and cone signals has been hampered by the presence of intimate physical and functional connections between rod and cone pathways. By deleting the cyclic nucleotide-gated channel CNG3 we have generated a mouse lacking any cone-mediated photoresponse. In contrast, the rod pathway is completely intact in CNG3-deficient mice. The functional loss of cone function correlates with a progressive degeneration of cone photoreceptors but not of other retinal cell types. CNG3-deficient mice provide an animal model to dissect unequivocally the contribution of rod and cone pathways for normal retinal function.