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Abstract #13115 Published in IGR 7-3
Study of effects of antiglaucoma eye drops on N-methyl-d: -aspartate-induced retinal damage
Metoki T; Ohguro H; Ohguro I; Mamiya K; Ito T; Nakazawa MJapanese Journal of Ophthalmology 2005; 49: 453-461
PURPOSE: To study the effects of antiglaucoma eye drops on N-methyl-D: -aspartate (NMDA)-induced retinal damage. METHODS: Several antiglaucoma eye drops, β-blockers, alpha/beta-blockers, an α1-blocker, an α2-agonist, and a prostaglandin derivative, were topically administrated to NMDA-treated rat eyes daily for 2 weeks, and the retinal thickness, the number of retrograde-labeled retinal ganglion cells (RGCs), and the results of a cDNA microarray analysis were studied. RESULTS: Intravitreal administration of NMDA caused a significant decrease in the thickness of the retinal layers and induced upregulation of glial fibrillary acidic protein (GFAP). Topical administration of β-blockers (timolol, betaxolol, and carteolol) and a prostaglandin derivative (latanoprost) showed almost no significant effects on retinal thickness, the number of RGCs, or expression of GFAP. In contrast, the alpha/beta-blockers (nipradilol and levobunolol), the α1-blocker (bunazosin HCl), and the α2-agonist (brimonidine) showed preservation effects on retinal thickness and the number of RGCs, and marked suppression of NMDA-induced upregulation of GFAP. Among 1101 genes related to cellular regulatory mechanisms, the expression of two genes, both for insulin-like growth factors, (IGF-1) and ErbB3, was altered upon administration of the alpha/beta-blockers, the α1-blocker, and the α2-agonist. CONCLUSION: Our present study suggests that modulations of the α-adrenergic receptor, α1-blocking and α2-stimulation, by antiglaucoma eye drops may cause beneficial effects on NMDA-induced retinal damage in the rat.
Dr. T. Metoki, Department of Ophthalmology, Hirosaki University School of Medicine, Hirosaki, Japan. ooguro@cc.hirosaki-u.ac.jp.
Classification:
11.8 Neuroprotection (Part of: 11 Medical treatment)