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J.L. Kielczewski, H.A. Quigley, M.E. Pease; The Effect of Experimental Glaucoma and Optic Nerve Transection on Amacrine Cells in Rat Retina . Invest. Ophthalmol. Vis. Sci. 2005;46(13):1237.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: To detect alterations in amacrine cells associated with retinal ganglion cell (RGC) depletion caused by experimental optic nerve transection and glaucoma. Methods: Intraocular pressure (IOP) was elevated unilaterally in the left eye of 18 animals by translimbal trabecular laser treatment for 1 month (n=6), 2 months (n=5), and 3 months (n=7). Full optic nerve transection was performed unilaterally in 9 rats with 1 month (n=4) and 3 month (n=5) survival. Serial cryosections (5 per eye) were immunohistochemically stained with rabbit anti–GABA and anti–glycine antibodies and peroxidase–conjugated secondaries. Cells in the ganglion cell and inner plexiform layers that were clearly labeled for GABA or glycine were counted in a masked fashion under brightfield microscopy. Results: The number of labeled amacrines was statistically unchanged after 1, 2 or 3 months of experimental glaucoma (557 + 186 amacrines/sqmm retina vs 664 + 114 in normals, p = 0.15, t test). Transection of the nerve caused significant decrease in amacrine labeling in both transected and fellow eyes 3 months after injury (72% decrease, p < 0.0001). Counts of remaining neurons in the ganglion cell layer in 3 month transected eyes suggest that amacrine cells were still present, though their GABA and glycine labeling was dramatically decreased. Conclusions: Minimal change in the number of amacrine cells occurs in experimental glaucoma. With massive RGC death after nerve transection, neurotransmitter presence is severely curtailed, but cell bodies appear to remain. Differences among optic nerve injury models and effects on "untreated" fellow eyes should be recognized.
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