Rearrangement of the cone mosaic in the retina of the rat model of retinitis pigmentosa.
Rearrangement of the cone mosaic in the retina of the rat model of retinitis pigmentosa.
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DOI：
10.1002/cne.22800
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发表时间：
2012-03-01
影响因子：
2.5
通讯作者：
Lee, Eun-Jin
中科院分区：
文献类型：
--
作者：
Ji, Yerina;Zhu, Colleen L.;Grzywacz, Norberto M.;Lee, Eun-Jin
在视网膜色素变性（RP）中，视锥细胞的死亡通常在视杆细胞变性后一段时间发生。最近，RP中存活的视锥细胞已被详细研究和报道。这些视锥在其形态上经历广泛的重塑。在这里，我们报告了一个扩展的重塑研究，考虑可能的修改空间分布模式。为此，我们使用了S334 ter-line-3转基因大鼠，一种表达导致RP的视紫红质突变的转基因模型。在本研究中，在出生后（P）P5-30、90、180和P600天收集视网膜。然后，我们对视网膜进行免疫染色，以检查视锥细胞的形态和分布，并量化总视锥细胞数。我们的研究结果表明，视锥细胞在其空间分布上发生了广泛的变化，从而产生了一个由有序的环阵列组成的马赛克。这些环首先开始出现在P15的视网膜随机区域，并在P90时遍布整个组织。这种分布模式在P180时失去清晰度，并在P600时大部分消失，此时锥细胞几乎全部死亡。相反，RP和正常条件下的视锥细胞的数量在晚至P180的阶段没有显示出显着差异。因此，环不是通过其中心的细胞死亡形成的，而是通过视锥细胞迁移形成的。我们讨论了其可能的机制，并建议热点杆死亡和Müller细胞的过程中的光感受器的低密度区的重塑的作用。
In retinitis pigmentosa (RP), the death of cones normally follows some time after the degeneration of rods. Recently, surviving cones in RP have been studied and reported in detail. These cones undergo extensive remodeling in their morphology. Here we report an extension of the remodeling study to consider possible modifications of spatial-distribution patterns. For this purpose we used S334ter-line-3 transgenic rats, a transgenic model developed to express a rhodopsin mutation causing RP. In this study, retinas were collected at postnatal (P) days P5–30, 90, 180, and P600. We then immunostained the retinas to examine the morphology and distribution of cones and to quantify the total cone numbers. Our results indicate that cones undergo extensive changes in their spatial distribution to give rise to a mosaic comprising an orderly array of rings. These rings first begin to appear at P15 at random regions of the retina and become ubiquitous throughout the entire tissue by P90. Such distribution pattern loses its clarity by P180 and mostly disappears at P600, at which time the cones are almost all dead. In contrast, the numbers of cones in RP and normal conditions do not show significant differences at stages as late as P180. Therefore, rings do not form by cell death at their centers, but by cone migration. We discuss its possible mechanisms and suggest a role for hot spots of rod death and the remodeling of Müller cell process into zones of low density of photoreceptors.
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