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1From the Department of Ophthalmology and Visual Sciences, The Chinese University of Hong Kong, Kowloon, Hong Kong; the 2Department of Ophthalmology, Doheny Eye Institute, Keck School of Medicine, University of Southern California, Los Angeles, California; the 3Glaucoma Division, Department of Ophthalmology, Jules Stein Eye Institute, University of California at Los Angeles School of Medicine, Los Angeles, California; and 4The Wilmer Ophthalmological Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland.
PURPOSE. To study the responses of glial cells to a short-term elevation in intraocular pressure (IOP) in rats.
METHODS. Adult Sprague-Dawley albino rats, 45 to 55 days old, were given India ink intracamerally. After 7 days, 200 spots of laser burn over 360° were delivered by an Argon laser (620–637 nm; 200 mW; 200 mm; 0.2 seconds) aimed at the ink deposits in the trabecular meshwork. IOP was recorded and eye tissues at 12 hours and 1, 3, 5, 7, or 14 days after laser were examined by immunohistochemistry with antibodies against glial fibrillary acidic protein (GFAP), vimentin, S-100, ED1, and OX42. To evaluate neuronal loss, the number of cells in the retinal ganglion cell layer (RGCL) was counted on flat preparations of retinas at various times after elevation of IOP.
RESULTS. Significant elevation of IOP from 1 to 7 days and loss of cells in the RGCL from 3 days onward were noted after trabecular laser photocoagulation. In the inner retina, there was a gradual and sustained increase in GFAP and S-100 immunoreactivity, but only a transient increase in vimentin immunoreactivity. No remarkable changes in GFAP, vimentin, and S-100 immunoreactivity were noted at the optic nerve head (ONH). ED1- and OX42-labeled cells were noted in the choroidal plexus, the parapapillary region of the optic nerve, and the ONH from 3 days onward, whereas expression in the retina was unremarkable.
CONCLUSIONS. There is differential expression of glial cell markers in the retina and the ONH, with early loss of cells in the RGCL in response to the elevation of IOP. Macroglia such as astrocytes and Müller cells may be involved in the pathophysiology of retinal ganglion cell death or retinal repair, and activated microglial/phagocytic cells may play an important role in modulating the changes in the ONH that occur with the elevation of IOP.
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