Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
Board

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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Poster Number PAayoub0171
Keywords: retina, glia, glutamate, transport, glaucoma