Ophthalmology Poster Session
McGhie, E (Dept of Biology, Westmont College, Santa Barbara, USA)
Schultz, L (Dept of Biology, Westmont College, Santa Barbara, USA)
Weinreb, R (Dept of Ophthalmology, UCSD, La Jolla, USA)
Lindsey, J (Dept of Ophthalmology, UCSD, La Jolla, USA)
Maguire, G (Dept of Ophthalmology, UCSD, La Jolla, USA)
Under ischemic conditions, glutamate is released into the CNS and induces neurotoxicity. The possible mechanisms releasing this glutamate are thought to be calcium-dependent, vesicular glutamate release, and calcium-independent reversed transport. Previous studies have suggested that glial cells, but not neurons can release glutamate by reversed transport. Here, using fluorometric imaging techniques in mouse and rat retina, we measured increased release of endogenous glutamate from retinal slices and isolated retinal cells under ischemic conditions showing that a dense cloud of glutamate, sufficient to induce long-term glutamate toxicity in retinal ganglion cells, is released in the area of the ganglion cell somata. Our data suggest that reversed transport of glutamate occurs in glial cells, but that it does not occur in neurons and that the primary source of the glutamate cloud surrounding the ganglion cell somata during ischemic conditions is through reversed transport of glutamate from retinal glial cells. Supported by NIH grants: #EY09173 (GSA) & #EY09133(GM), The Glaucoma Foundation (GM), and The Foundation for Eye Research (GSA, GM).
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|Ayoub, G; McGhie, E; Schultz, L; Weinreb, R; Lindsey, J; Maguire, G; (1998). Glutamate and Glaucoma: Glutamate is released by reverse transport from retinal glial cells and not neurons. Presented at INABIS '98 - 5th Internet World Congress on Biomedical Sciences at McMaster University, Canada, Dec 7-16th. Available at URL http://www.mcmaster.ca/inabis98/ophthalmology/ayoub0171/index.html|
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