Role of Retinal Glial Cells in Nitric Oxide and Glutamate Toxicity in Glaucoma

Theresa Good, PhD
Texas Engineering Experiment Statio (College Station, TX)
Year Awarded:
2001
Grant Duration:
April 1, 2001 to March 31, 2003
Disease:
Glaucoma
Award Amount:
$58,694
Grant Reference ID:
G2001009
Award Type:
Standard
Award Region:
US Southern

Role of Retinal Glial Cells in Nitric Oxide and Glutamate Toxicity in Glaucoma

Details

When IOP is elevated, the lamina cribrosa (the part of the eye that the optic nerve passes through) becomes deformed and the cells within the tissue get stretched. Dr. Good has used a mathematical model to estimate the degree of cell deformation within the retina and then built an apparatus (in vitro model) to stretch cells to the same extent that they would be stretched during glaucoma. She has found that the deformation of retinal glial cells leads to the permeability of the cells, the release of glutamate and the production of large amounts of nitric oxide. The release of nitric oxide and glutamate could kill retinal ganglion cells and lead to vision loss. She is now examining the mechanism by which the deformation of cells leads to glutamate release and nitric oxide production. She is also examining how excess levels of both of these compounds could kill the cells within the optic nerve. She will then explore ways in which glutamate release and nitric oxide production could be prevented and see if they will spare cells that make up the optic nerve in culture. This project is a continuation of Dr. Good's previous BrightFocus-funded study, Role of Glial Cells in Retinal Ganglion Cell Death, begun in 1999.
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