Eichhorn M, Schreckenberger M, Tamm E R, Lütjen-Drecoll E
Anatomisches Institut, Lehrstuhl II, Universität Erlangen-Nürnberg, Germany.
Graefes Arch Clin Exp Ophthalmol. 1996 Apr;234(4):258-63. doi: 10.1007/BF00430419.
In Royal College of Surgeons (RCS) rats the retinal pigmented epithelium (RPE) exhibits defective phagocytosis of rod outer segments, causing degeneration of the photoreceptor layer. It is not known whether another function of the RPE, ion and fluid transport, is also affected by the disease. One enzyme involved in modulation of RPE transport activities is carbonic anhydrase (CA). To clarify whether changes in CA activity are correlated with the process of retinal degeneration, the localization of CA activity in RCS rat eyes was investigated.
Eyes of 12 RCS rats and 12 age-matched congenic controls of different ages were studied, using a modified histochemical method of Hansson for light and electron microscopy.
Control eyes showed CA staining in corneal endothelium, both layers of ciliary epithelium, Müller cells, inner segments of photoreceptors, and RPE cells. In RPE the apical membranes were most intensely stained. In RCS rats, changes in CA staining were seen only in the posterior segment of rats 6 and 7 months of age. Most of the RPE cells were more intensely stained than those of age-matched controls, especially due to increased CA activity in the basolateral membrane infoldings. Adjacent endothelial cells of the choriocapillaris and of retinal capillaries developed staining for CA activity.
Changes in CA activity in the RPE and adjacent capillary endothelium, together with previously described changes in RPE morphology in RCS rats, indicate changes in ion and fluid transport across the RPE. Since the retina was already impaired when the increase in CA activity occurred, we hypothesize that the causative factor is not the genetic defect per se, but the destruction of the retina.
在皇家外科学院（RCS）大鼠中，视网膜色素上皮（RPE）对视杆细胞外节的吞噬作用存在缺陷，导致光感受器层退化。目前尚不清楚RPE的另一功能——离子和液体转运是否也受该疾病影响。参与调节RPE转运活动的一种酶是碳酸酐酶（CA）。为了阐明CA活性的变化是否与视网膜变性过程相关，研究了RCS大鼠眼中CA活性的定位。
使用改良的汉森组织化学方法对12只RCS大鼠和12只不同年龄的年龄匹配同基因对照大鼠的眼睛进行光镜和电镜研究。
对照眼在角膜内皮、睫状体上皮的两层、米勒细胞、光感受器的内节和RPE细胞中显示出CA染色。在RPE中，顶端膜染色最强烈。在RCS大鼠中，仅在6个月和7个月大的大鼠后段观察到CA染色的变化。大多数RPE细胞比年龄匹配的对照细胞染色更强，特别是由于基底外侧膜褶皱处的CA活性增加。脉络膜毛细血管和视网膜毛细血管的相邻内皮细胞出现了CA活性染色。
RPE和相邻毛细血管内皮中CA活性的变化，以及先前描述的RCS大鼠RPE形态的变化，表明跨RPE的离子和液体转运发生了变化。由于CA活性增加时视网膜已经受损，我们推测致病因素不是遗传缺陷本身，而是视网膜的破坏。
