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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Nonvisual light responses in the Rpe65 knockout mouse: Rod loss restores sensitivity to the melanopsin system
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Nonvisual light responses in the Rpe65 knockout mouse: Rod loss restores sensitivity to the melanopsin system

机译：Rpe65基因敲除小鼠的非视觉光反应：视杆丧失可恢复对黑色素系统的敏感性

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摘要

Intrinsically photosensitive retinal ganglion cells (ipRGCs) expressing the photopigment melanopsin (OPN4), together with rods and cones, provide light information driving nonvisual light responses. We examined nonvisual photoreception in mice lacking RPE65, a protein that is required for regeneration of visual chromophore in rods and cones. Although Rpe65 knockouts retain a small degree of rod function, we show here that circadian phase shifting responses in Rpe65(-/-) mice are attenuated far beyond what has been reported for rodless/coneless mice. Furthermore, the number of melanopsin-immunoreactive perikarya and the extent of dendritic arborizations were decreased in Rpe65 knockout mice compared with controls. To assess the nature of the photoreceptive defect in Rpe65 null mice, we eliminated either rods or melanopsin from Rpe65(-/-) retinas by generating (i) Rpe65(-/-) mice carrying a transgene (rdta) that results in selective elimination of rods and (h) double knockout Rpe65(-/-);Opn4(-/-) mice. Surprisingly, rod loss in Rpe65 knockout mice resulted in restoration of circadian photosensitivity. Normal photoentrainment was lost in Rpe65(-/-); Opn4(-/-) mice, and, instead, a diurnal phenotype was observed. Our findings demonstrate that RPE65 is not required for ipRGC function but reveal the existence of a mechanism whereby rods may influence the function of ipRGCs.
机译：表达光色素黑素（OPN4）以及棒和视锥细胞的内在光敏性视网膜神经节细胞（ipRGC）提供驱动非视觉光响应的光信息。我们在缺乏RPE65的小鼠中检查了非视觉光感受，RPE65是视杆和视锥中生色团的再生所必需的蛋白质。尽管Rpe65基因敲除保留了很小程度的杆功能，我们在这里显示Rpe65（-/-）小鼠的昼夜节律相移响应衰减远超过无杆/无锥小鼠的报道。此外，与对照组相比，Rpe65基因敲除小鼠的黑素视蛋白免疫反应性果核的数量和树突状乔化的程度均降低。为了评估Rpe65无效小鼠中光感受器缺陷的性质，我们通过产生（i）携带转基因（rdta）导致选择性消除的Rpe65（-/-）小鼠消除了Rpe65（-/-）视网膜中的视杆或黑色素。杆和（h）双敲除Rpe65（-/-）; Opn4（-/-）小鼠。出人意料的是，Rpe65基因敲除小鼠的杆丢失导致昼夜节律性光敏性恢复。在Rpe65（-/-）中失去了正常的光夹带； Opn4（-/-）小鼠，相反，观察到昼夜表型。我们的发现表明RPE65不是ipRGC功能所必需的，但揭示了杆可能影响ipRGCs功能的机制的存在。

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