Szczesny Piotr
I Kliniki Okulistyki Akademii Medycznej w Lublinie.
Klin Oczna. 2002;104(3-4):195-200.
It has been suggested that structural alterations of the photoreceptor connecting cilium are a primary defects leading to photoreceptor degeneration in some forms of inherited retinal degenerations (5). In a series of 17 eyes with retinitis pigmentosa (RP) and with various genetic forms of RP, examined by electron microscopy, no structural abnormalities were found in the arrangement of the ciliary microtubules. However, a 10% reduction in the ciliary diameter was recorded in RP photoreceptors (12). The question arose: is thinning of the cilium a primary defect associated with RP, or a secondary abnormality related to degenerative processes in photoreceptors irrespective of the cause? The aim of this study was to examine the photoreceptor connecting cilia in the early stages of experimental light induced retinal degeneration in the rat, by conducting a structural and morphometric survey of the relevant electron-micrographs. In addition, the effects of various fixation techniques on the ciliary structure were compared.
Analysis of 124 transmission electron micrographs of 9 controls and 155 transmission electron micrographs of 55 light damaged animals was conducted. For the effects of fixation on morphometry 72 transmission electron micrographs from an additional 4 controls (43 negatives) and 8 light damaged animals (29 negatives) were examined. Light damage was induced by exposure to 1000 lux of white light for 120 minutes. Retinal samples were fixed either in 2.5% glutaraldehyde or by high pressure freezing followed by freeze-substitution.
This study showed that one of the early morphological alterations occurring in rat photoreceptors damaged by light is a reduction of ciliary diameter of approximately 10%. It was not associated with any apparent ultrastructural changes in the axoneme. It was also found that the degree of ciliary shrinkage largely depends on the fixation technique used. Cryo-fixation followed by freeze substitution shows more shrinkage than chemical fixation by immersion in glutaraldehyde.
It is suggested, that reduction in photoreceptor cilium diameter is a secondary and non-specific change. It is not a unique phenomenon, observed not only in human photoreceptors, which are undergoing degeneration in RP. It can be induced in otherwise healthy rat retina, in which photoreceptor degeneration was caused by exposure to toxic levels of light.
有人提出,光感受器连接纤毛的结构改变是导致某些形式遗传性视网膜变性中光感受器退化的主要缺陷(5)。在一系列17只患有色素性视网膜炎(RP)且具有各种RP遗传形式的眼睛中,通过电子显微镜检查,未发现睫状微管排列存在结构异常。然而,在RP光感受器中记录到睫状体直径减小了10%(12)。问题出现了:睫状体变细是与RP相关的主要缺陷,还是与光感受器退化过程相关的继发性异常,而与病因无关?本研究的目的是通过对相关电子显微镜照片进行结构和形态测量调查,检查大鼠实验性光诱导视网膜变性早期阶段的光感受器连接纤毛。此外,比较了各种固定技术对睫状结构的影响。
对9只对照动物的124张透射电子显微镜照片和55只光损伤动物的155张透射电子显微镜照片进行了分析。为了研究固定对形态测量的影响,检查了另外4只对照动物(43张阴性照片)和8只光损伤动物(29张阴性照片)的72张透射电子显微镜照片。通过暴露于1000勒克斯的白光下120分钟诱导光损伤。视网膜样本用2.5%戊二醛固定或通过高压冷冻然后冷冻置换进行固定。
本研究表明,大鼠光感受器受光损伤后早期发生的形态学改变之一是睫状体直径减小约10%。这与轴丝中任何明显的超微结构变化无关。还发现睫状体收缩程度在很大程度上取决于所使用的固定技术。冷冻固定然后冷冻置换显示出比通过浸入戊二醛进行化学固定更多的收缩。
有人提出,光感受器睫状体直径减小是一种继发性非特异性变化。它不是一种独特的现象,不仅在RP中正在退化的人类光感受器中观察到。在原本健康的大鼠视网膜中也可诱导这种现象,其中光感受器退化是由暴露于有毒水平的光引起的。