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D. C. Fernandez, M. S. Chianelli, R. E. Rosenstein; Involvement of Glutamate in Retinal Protection Against Ischemia/Reperfusion Damage Induced by Post-Conditioning. Invest. Ophthalmol. Vis. Sci. 2010;51(13):4699.
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Retinal ischemia could provoke blindness and there is no effective treatment against retinal ischemic damage. Brief intermittent ischemia applied during the onset of reperfusion (i.e., post-conditioning) protects the retina from ischemia/reperfusion injury. Multiple evidences support that glutamate is implicated in retinal ischemic damage. We investigated the involvement of glutamate clearance in post-conditioning-induced protection.
Ischemia was induced in male Wistar rats by increasing intra-ocular pressure (120 mm Hg for 40 min), and 5 min after reperfusion, animals underwent seven cycles of 1 min/1 min ischemia/reperfusion. One, three, or seven days after ischemia, animals were subjected to electroretinography , histological and biochemical analysis.
The functional and histological protection induced by post-conditioning was evident at 7 (but not 1 or 3) days post-ischemia. An increase in Müller cell glial fibrillary acidic protein (GFAP) levels was observed at 1, 3, and 7 days after ischemia, whereas post-conditioning reduced GFAP levels of Müller cells at 3 and 7 days post-ischemia. Three days after ischemia, a significant decrease in glutamate uptake and glutamine synthetase activity was observed, whereas post-conditioning reversed the effect of ischemia. The intravitreal injection of supraphysiological levels of glutamate mimicked electroretinographic and histological alterations provoked by ischemia, which were abrogated by post-conditioning.
These results support the involvement of glutamate in retinal protection against ischemia/reperfusion damage induced by post-conditioning.
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