M. Eichhorn et al., CARBONIC-ANHYDRASE ACTIVITY IS INCREASED IN RETINAL PIGMENTED EPITHELIUM AND CHORIOCAPILLARIS OF RCS RATS, Graefe's archive for clinical and experimental ophthalmology, 234(4), 1996, pp. 258-263
Background: In Royal College of Surgeons (RCS) rats the retinal pigmen
ted epithelium (RPE) exhibits defective phagocytosis of rod outer segm
ents, 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 tra
nsport activities is carbonic anhydrase (CA). To clarify whether chang
es in CA activity are correlated with the process of retinal degenerat
ion, the localization of CA activity in RCS rat eyes was investigated.
Methods: 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. Results: Control eyes showe
d CA staining in corneal endothelium, both layers of ciliary epitheliu
m, Muller cells, inner segments of photoreceptors, and RPE cells. In R
PE the apical membranes were most intensely stained. In RCS rats, chan
ges in CA staining were seen only in the posterior segment of rats 6 a
nd 7 months of age. Most of the RPE cells were more intensely stained
than those of age-matched controls, especially due to increased CA act
ivity in the basolateral membrane infoldings. Adjacent endothelial cel
ls of the choriocapillaris and of retinal capillaries developed staini
ng for CA activity. Conclusion: Changes in CA activity in the RPE and
adjacent capillary endothelium, together with previously described cha
nges in RPE morphology in RCS rats, indicate changes in ion and fluid
transport across the RPE. Since the retina was already impaired when t
he increase in CA activity occurred, we hypothesize that the causative
factor is not the genetic defect per se, but the destruction of the r
etina.