- Involvement of glutamate in retinal protection against ischemia/reperfusion damage induced by post-conditioning.

FERNANDEZ, DC; CHIANELLI, MS; ROSENSTEIN, RE

Fort Lauderdale

Congreso; The Association for Research in Vision and Ophthalmology; 2010

The Association for Research in Vision and Ophthalmology

Invest Ophthalmol Vis Sci 2010;51: E-Abstract 4699.© 2010 ARVO 4699—D1037 Involvement of Glutamate in Retinal Protection Against Ischemia/Reperfusion Damage Induced by Post-Conditioning D. C. Fernandez, M. S. Chianelli and R. E. Rosenstein Dept Human Biochem-Sch Med, University of Buenos Aires, Buenos Aires, Argentina Commercial Relationships: D.C. Fernandez, None; M.S. Chianelli, None; R.E. Rosenstein, None. Support: ANPCyT PICT 2006 1623, CONICET Abstract Purpose: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. Methods: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. Results: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. Conclusions:These results support the involvement of glutamate in retinal protection against ischemia/reperfusion damage induced by post-conditioning. Keywords: retina: neurochemistry • excitatory neurotransmitters • Muller cells