Mechanism of the pathogenesis of glutamate neurotoxicity in retinal ischemia

K Adachi, S Kashii, H Masai, M Ueda… - Graefe's archive for …, 1998 - Springer
K Adachi, S Kashii, H Masai, M Ueda, C Morizane, K Kaneda, T Kume, A Akaike, Y Honda
Graefe's archive for clinical and experimental ophthalmology, 1998Springer
Abstract· 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 ω-nitro-l-arginine methyl ester), and D-NAME (N
ω-nitro-d-arginine methyl ester) on the histological changes in the rat retina induced by …
Abstract
· 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 ω-nitro-l-arginine methyl ester), and D-NAME (N ω-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.
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