Immunohistochemical features of cells in peripheral microcystoid retinal degeneration

Abstract

Peripheral microcystoid retinal degeneration (PMD) is an age-related, benign condition in which the peripheral retina develops small holes and undergoes cystic degeneration. This paper demonstrates neuronal alterations in PMD, as studied by immunohistochemistry in postmortem donor eyes (age: 76–89 years; N = 6 donors). In all cases, the degeneration was located in the inferior temporal quadrant, creating holes in the far peripheral retina. There was thinning of the inner retinal layers and the outer plexiform layer (OPL) was patchy or inconspicuous. As a response, Müller cell processes showed increased vimentin immunoreactivity. None of the retinas examined expressed glial fibrillary acidic protein. Cone photoreceptor cells were significantly altered: compared to the adjoining cones that were short, those located in the cystoid retina underwent significant elongation of their inner segments, evident from calbindin immunolabeling, to maintain synaptic contacts with the remnant OPL. The latter consisted of small photoreceptor terminals and scanty processes from shrunken bipolar cells. Besides, cones and ganglion cells undergo oxidative stress, they showed immunoreactivity to 4-hydroxy 2-nonenal and nitrotyrosine. The level of superoxide dismutase-2 was relatively low in the PMD region than in adjacent area, suggesting that the former suffers from oxidative stress.