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Rita Naskar, Christian K. Vorwerk, Evan B. Dreyer; Concurrent Downregulation of a Glutamate Transporter and Receptor in Glaucoma. Invest. Ophthalmol. Vis. Sci. 2000;41(7):1940-1944.
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purpose. Elevated levels of extracellular glutamate have been implicated in the
pathophysiology of neuronal loss in both central nervous system and
ophthalmic disorders, including glaucoma. This increase in glutamate
may result from a failure of glutamate transporters, which are
molecules that ordinarily regulate extracellular glutamate. Elevated
glutamate levels can also lead to a perturbation in glutamate
receptors. The hypothesis for the current study was that glutamate
transporters and/or receptors are altered in human glaucoma.
methods. Immunohistochemical analyses of human eyes with glaucoma and control
eyes were performed to evaluate glutamate receptors and transporters.
These molecules were also assayed in rat eyes injected with
glial-derived neurotrophic factor (GDNF).
results. Glaucomatous eyes had decreased levels of both the glutamate
transporter, excitatory amino acid transporter (EAAT)-1, and the
glutamate receptor subunit N-methyl-d-aspartate
(NMDA)-R1. Eyes treated with GDNF had elevated levels of both EAAT1 and
conclusions. The loss of EAAT1 in glaucoma may account for the elevated level of
glutamate found in glaucomatous vitreous and lead to a compensatory
downregulation of NMDAR1. Inasmuch as GDNF can increase levels of both
EAAT1 and NMDAR1, it may be a useful therapeutic approach to restore
homeostatic levels of these in glaucoma.
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