PURPOSE: This study was carried out to examine the involvement of glutamate and nitric oxide neurotoxicity in ischemia/reperfusion-induced retinal injury in vivo. METHODS: We monitored glutamate release from in vivo cat retina during and after pressure-induced ischemia using a microdialysis technique. Morphometric studies were performed to study the effects of MK-801 (dizocilpine), L-NAME (N omega-nitro-L-arginine methyl ester), and D-NAME (N omega-nitro-D-arginine methyl ester) on the histological changes in the rat retina induced by ischemia or intravitreal injection of NMDA (N-methyl-D-aspartate; 200 nmol). RESULTS: A large release of glutamate occurred during ischemia, followed by a marked release after reperfusion. Histological changes occurred selectively in the inner part of the retina after ischemia as well as intravitreal injection of NMDA. Pretreatment with intravenous injection of MK-801 or L-NAME significantly inhibited the ischemic injury of the inner retina. Intravitreal injection of L-NAME inhibited NMDA-induced neurotoxicity in the retina. CONCLUSION: These findings indicate that nitric oxide mediates neurotoxic actions of glutamate which are responsible for ischemic injury in the retina.
PURPOSE: This study was carried out to examine the involvement of glutamate and nitric oxideneurotoxicity in ischemia/reperfusion-induced retinal injury in vivo. METHODS: We monitored glutamate release from in vivo cat retina during and after pressure-induced ischemia using a microdialysis technique. Morphometric studies were performed to study the effects of MK-801 (dizocilpine), L-NAME (N omega-nitro-L-arginine methyl ester), and D-NAME (N omega-nitro-D-arginine methyl ester) on the histological changes in the rat retina induced by ischemia or intravitreal injection of NMDA (N-methyl-D-aspartate; 200 nmol). RESULTS: A large release of glutamate occurred during ischemia, followed by a marked release after reperfusion. Histological changes occurred selectively in the inner part of the retina after ischemia as well as intravitreal injection of NMDA. Pretreatment with intravenous injection of MK-801 or L-NAME significantly inhibited the ischemic injury of the inner retina. Intravitreal injection of L-NAME inhibited NMDA-induced neurotoxicity in the retina. CONCLUSION: These findings indicate that nitric oxide mediates neurotoxic actions of glutamate which are responsible for ischemic injury in the retina.
Authors: Leon C Ho; Bo Wang; Ian P Conner; Yolandi van der Merwe; Richard A Bilonick; Seong-Gi Kim; Ed X Wu; Ian A Sigal; Gadi Wollstein; Joel S Schuman; Kevin C Chan Journal: Invest Ophthalmol Vis Sci Date: 2015-06 Impact factor: 4.799
Authors: Anne Katrine Toft-Kehler; Dorte Marie Skytt; Kristian Arild Poulsen; Charlotte Taul Brændstrup; Georgi Gegelashvili; Helle Waagepetersen; Miriam Kolko Journal: Neurochem Res Date: 2014-04-04 Impact factor: 3.996