Montalbán-Soler Luis, Alarcón-Martínez Luis, Jiménez-López Manuel, Salinas-Navarro Manuel, Galindo-Romero Caridad, Bezerra de Sá Fabrízio, García-Ayuso Diego, Avilés-Trigueros Marcelino, Vidal-Sanz Manuel, Agudo-Barriuso Marta, Villegas-Pérez Maria P
Departamento de Oftalmología, Optometría, Otorrinolaringología y Anatomía Patológica, Facultad de Medicina, Universidad de Murcia, Murcia, Spain.
Mol Vis. 2012;18:675-93. Epub 2012 Mar 24.
To investigate the anatomic and functional changes triggered by light exposure in the albino mouse retina and compare them with those observed in the albino rat.
BALB/c albino mice were exposed to 3,000 lx of white light during 24 h and their retinas analyzed from 1 to 180 days after light exposure (ALE). Left pupil mydriasis was induced with topical atropine. Retinal function was analyzed by electroretinographic (ERG) recording. To assess retinal degeneration, hematoxylin and eosin staining, the TdT-mediated dUTP nick-end labeling (TUNEL) technique, and quantitative immunohistofluorescence for synaptophysin and protein kinase Cα (PKCα) were used in cross sections. Intravenous injection of horseradish peroxidase and Fluoro-Gold™ tracing were used in whole-mounted retinas to study the retinal vasculature and the retinal ganglion cell (RGC) population, respectively.
Light exposure caused apoptotic photoreceptor death in the central retina. This death was more severe in the dorsal than in the ventral retina, sparing the periphery. Neither retinal vascular leakage nor retinal ganglion cell death was observed ALE. The electroretinographic a-wave was permanently impaired, while the b-wave decreased but recovered gradually by 180 days ALE. The scotopic threshold responses, associated with the inner retinal function, diminished at first but recovered completely by 14 days ALE. This functional recovery was concomitant with the upregulation of protein kinase Cα and synaptophysin. Similar results were obtained in both eyes, irrespective of mydriasis.
In albino mice, light exposure induces substantial retinal damage, but the surviving photoreceptors, together with compensatory morphological/molecular changes, allow an important restoration of the retinal function.
研究光照对白化病小鼠视网膜引发的解剖学和功能变化，并将其与白化病大鼠中观察到的变化进行比较。
将BALB/c白化病小鼠暴露于3000勒克斯的白光下24小时，并在光照后1至180天（ALE）对其视网膜进行分析。用局部阿托品诱导左瞳孔散大。通过视网膜电图（ERG）记录分析视网膜功能。为评估视网膜变性，在横切面上使用苏木精和伊红染色、TdT介导的dUTP缺口末端标记（TUNEL）技术以及对突触素和蛋白激酶Cα（PKCα）的定量免疫荧光。在整个视网膜标本中分别静脉注射辣根过氧化物酶和Fluoro-Gold™示踪剂，以研究视网膜血管系统和视网膜神经节细胞（RGC）群体。
光照导致中央视网膜中的光感受器凋亡性死亡。这种死亡在背侧视网膜比腹侧视网膜更严重，周边区域未受影响。在ALE时未观察到视网膜血管渗漏或视网膜神经节细胞死亡。视网膜电图的a波永久性受损，而b波降低，但在ALE后180天逐渐恢复。与视网膜内层功能相关的暗视阈值反应起初降低，但在ALE后14天完全恢复。这种功能恢复与蛋白激酶Cα和突触素的上调同时发生。无论瞳孔散大与否，双眼均获得相似结果。
在白化病小鼠中，光照会引起显著的视网膜损伤，但存活的光感受器以及代偿性的形态学/分子变化使得视网膜功能得到重要恢复。
