Immunohistologic evidence for retinal glial cell changes in human glaucoma.

PURPOSE Glial cells are structurally and functionally linked to neuronal tissues. Pathologically, the cells may be activated and characterized by increased size and number and altered cellular properties. In glaucoma, pathologic mechanisms within the anterior optic nerve may include glial activation. This study examines morphologic changes of glial cells in the retinas of glaucomatous eyes compared with age-matched control retinas. METHODS Paraffin-processed or flatmounted retinas from 17 human donor eyes [7 normal (donor age, 87.3 +/- 8.3 years) and 10 glaucomatous (donor age, 87.1 +/- 6.9 years)] were examined. With immunohistochemical methods, retinal glial cells were stained with an antibody to glial fibrillary acidic protein (GFAP). The morphology of the glial cells in normal and glaucomatous retinas was evaluated with fluorescence microscopy. RESULTS Three types of glial cells were identified in flatmounted retinas with differing distributions in the peripapillary region, the nerve fiber layer (NFL), and along the capillaries. Compared with normal eyes, in glaucomatous retinas the glial cells in the peripapillary region showed an increase in density and exhibited a deformation of the end feet. The astrocytes distributed among the NFL showed little difference from normal. The astrocytes accompanying the capillary bed showed a redistribution in the glaucomatous retinas. The quantification of glial cells in paraffin-processed glaucomatous retinas exhibited a profound increase in density and a significant increase of GFAP immunoreactivity in contrast to the lightly stained glial cells in normal retinas. CONCLUSIONS The activation of glial cells in the glaucomatous retina was characterized in changes of intensity of GFAP immunoreactivity and morphology around the larger blood vessels, compared with age-matched normal retinas. The relationships between glial cells, neuronal cells, and the vasculature, as well as the potential role of glial cells in pathologic mechanisms during different stages of neuronal damage in glaucoma, are discussed.