Involvement of Glutamate in Retinal Protection Against Ischemia/Reperfusion Damage Induced by Post-Conditioning

FERNANDEZ, DIEGO; CHIANELLI, MÓNICA; ROSENSTEIN RE

Fort Lauderdale, USA

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

The Association for Research in Vision and Ophthalmology

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 © 2010, The Association for Research in Vision and Ophthalmology, Inc., all rights reserved. Permission to republish any abstract or part of an abstract in any form must be obtained in writing from the ARVO Office prior to publication.