Benthal Molly C, McKeown Alex S, Kraft Timothy W
Department of Optometry, University of Alabama at Birmingham, 1720 2nd Ave South, Birmingham, AL 35294, USA.
Department of Vision Sciences, University of Alabama at Birmingham, 1720 2nd Ave South, Birmingham, AL 35294, USA.
Int J Mol Sci. 2022 Apr 2;23(7):3978. doi: 10.3390/ijms23073978.
We investigated the etiology of decreased cone-driven vision in a light damage (LD) model of retinal degeneration. To induce slow, moderate degeneration, albino rats underwent low-intensity light exposure for 10 days. Electroretinography was utilized to assess physiologic function of the rod- and cone-driven retinal function in LD and control rats. Immunohistochemistry targeting cone arrestin allowed for quantification of cone density and for comparison of the decline in function. Photoreceptor loss was quantified by outer nuclear layer thickness decreases, as observed by optical coherence tomography and histology. The LD rats showed decreased rod- and cone-driven function with partial recovery 30 days after cessation of light exposure. In addition, LD rats showed decreased cone photoreceptor densities in the central retinal region compared to control rats. Our results demonstrate that the loss of cone-driven visual function induced by light damage is at least partially due to the death of cone photoreceptors.
我们在视网膜变性的光损伤(LD)模型中研究了视锥细胞驱动视觉下降的病因。为诱导缓慢、中度变性,白化大鼠接受低强度光照10天。利用视网膜电图评估LD大鼠和对照大鼠中视杆和视锥细胞驱动的视网膜功能的生理功能。针对视锥细胞抑制蛋白的免疫组织化学可对视锥细胞密度进行定量,并比较功能下降情况。通过光学相干断层扫描和组织学观察到的外层核层厚度减少来量化光感受器损失。LD大鼠在停止光照30天后显示视杆和视锥细胞驱动功能下降且有部分恢复。此外,与对照大鼠相比,LD大鼠在视网膜中央区域的视锥光感受器密度降低。我们的结果表明,光损伤诱导的视锥细胞驱动视觉功能丧失至少部分是由于视锥光感受器的死亡。