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Mechanism of the pathogenesis of glutamate neurotoxicity in retinal ischemia.
Graefes Arch Clin Exp Ophthalmol. 1998 Oct; 236(10):766-74.GA

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 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+Show Affiliations

Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9801892

Citation

Adachi, K, et al. "Mechanism of the Pathogenesis of Glutamate Neurotoxicity in Retinal Ischemia." Graefe's Archive for Clinical and Experimental Ophthalmology = Albrecht Von Graefes Archiv Fur Klinische Und Experimentelle Ophthalmologie, vol. 236, no. 10, 1998, pp. 766-74.
Adachi K, Kashii S, Masai H, et al. Mechanism of the pathogenesis of glutamate neurotoxicity in retinal ischemia. Graefes Arch Clin Exp Ophthalmol. 1998;236(10):766-74.
Adachi, K., Kashii, S., Masai, H., Ueda, M., Morizane, C., Kaneda, K., Kume, T., Akaike, A., & Honda, Y. (1998). Mechanism of the pathogenesis of glutamate neurotoxicity in retinal ischemia. Graefe's Archive for Clinical and Experimental Ophthalmology = Albrecht Von Graefes Archiv Fur Klinische Und Experimentelle Ophthalmologie, 236(10), 766-74.
Adachi K, et al. Mechanism of the Pathogenesis of Glutamate Neurotoxicity in Retinal Ischemia. Graefes Arch Clin Exp Ophthalmol. 1998;236(10):766-74. PubMed PMID: 9801892.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mechanism of the pathogenesis of glutamate neurotoxicity in retinal ischemia. AU - Adachi,K, AU - Kashii,S, AU - Masai,H, AU - Ueda,M, AU - Morizane,C, AU - Kaneda,K, AU - Kume,T, AU - Akaike,A, AU - Honda,Y, PY - 1998/11/5/pubmed PY - 1998/11/5/medline PY - 1998/11/5/entrez SP - 766 EP - 74 JF - Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie JO - Graefes Arch Clin Exp Ophthalmol VL - 236 IS - 10 N2 - 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. SN - 0721-832X UR - https://www.unboundmedicine.com/medline/citation/9801892/Mechanism_of_the_pathogenesis_of_glutamate_neurotoxicity_in_retinal_ischemia_ L2 - https://dx.doi.org/10.1007/s004170050156 DB - PRIME DP - Unbound Medicine ER -