@phdthesis{oai:air.repo.nii.ac.jp:00002295,
 author = {神, 大介 and Jin, Daisuke},
 month = {Jun},
 note = {Purpose. To examine the involvement of nitric oxide (NO) in the development of ischemic retinal degeneration using glutamate receptor antagonists, inhibitors of nitric oxide syntheses (NOS), and NO donors. Methods. Simulated ischemia was induced in the rat ex vivo retinal preparations by deprivation of oxygen and glucose from the incubation medium. The NMDA receptor antagonist (MK-801) and non-NMDA receptor antagonist (GYKI) were applied to the ischemic retinal preparations in combination with different types of NOS inhibitors. The neuroprotective effects of these agents were evaluated by morphologically and biochemically. In addition, the deteriorating actions of NO donors to the control and ischemic retina were also examined. Results. Simulated ischemia produced severe acute neurodegeneration. This neurodegeneration was prevented by the combination of GYKI and MK-801. However, the NO donor induced severe retinal degeneration under the simulated ischemia, in spite of the co-administration of GYKI and MK-801. A neuronal NOS inhibitor offered substantial protection against neuronal damage combined with GYKI. Administration of NO donors invalidated the neuroprotective effects of MK-801and GYKI against the simulated ischemia. Conclusions. The present study revealed that the NO release after activation of glutamate receptors seems to play an important role in the neuronal cell death induced by ischemia.},
 school = {秋田大学},
 title = {Involvement of Nitric Oxide In Simulated Retinal Ischemia},
 year = {2014}
}