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J. Dong, J. Saugstad, L. Wang, G.A. Cioffi; Human Glaucoma Patients Exhibit Increased Expression of Group II Metabotropic Glutamate Receptors in the Optic Nerve . Invest. Ophthalmol. Vis. Sci. 2003;44(13):4411.
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Purpose: One mechanism underlying the pathophysiology of retinal ganglion cells in glaucoma may involve excitotoxic effects due to a chronic elevation of glutamate. Metabotropic glutamate receptors (mGluRs) may contribute to the pathophysiology of glaucoma through changes in protein expression levels or in the regulation of their responses due to the prolonged presence of increased glutamate. For this study, we examined the expression levels of the group II receptors, mGluR2 and mGluR3, in normal and glaucomatous eyes. Methods: Immunocytochemistry was performed on retinal and optic nerve sections from patients with primary open-angle glaucoma (Age: 86.5 ± 8.54; n=4) and age-matched normal subjects (Age: 85.5 ± 8.23; n=4). An antibody that detects both mGluR2 and mGluR3 was used to immunostain the sections, and protein levels were assessed by light microscopy. Glial cells were selectively labeled with the glial cell markers. Results: The results from the immunostaining of normal retinal sections were consistent with previous studies; the mGluR2/3 antibody labeled inner plexiform layer. However, There is no detectable change in the level of protein expression for mGluR2/3 between normal and glaucomatous retina. In contrast, glaucomatous eyes showed a much greater level of mGluR2/3 protein expression in the optic nerve than those from age-matched normal eyes. The optic nerve immunostaining of mGluR2/3 was mostly associated with oligodendroglial and/or microglial cells, but not astrocytes, and the staining exhibited regional and cellular differences. Conclusions: These data show the increased expression of mGluR2/3 in optic nerve, but not in retina, in glaucomatous eyes. It may reflect a role of these receptors as a cellular defense mechanism in response to injury. In addition, it supports the hypothesis that the pathophysiology underlying the death of ganglion cell axons in glaucoma might involve in glial-axon interactions.
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