@article{oai:niigata-u.repo.nii.ac.jp:00014182,
 author = {橋本, 薫},
 issue = {9},
 journal = {新潟医学会雑誌, 新潟医学会雑誌},
 month = {Sep},
 note = {It is well known that transient ischemic insult induces delayed neuronal cell death in the retina, probably due to disturbance of Ca^<2+> homeostasis triggered by excessive amounts of excitatory amino acids through glutamate recepter channels. To clarify how NMDA receptor channels are involved in the delayed neuronal cell death in the retina, we used the GluR ε 1 (NR 2 A) and GluR ε 2 (NR 2 B) subunits knockout mice for ischemia-reperfusion experiments. Transient retinal ischemia was generated by raising intraocular pressure up to about 120mmHg for 45-60 minutes under anesthesia. In the wild type, almost all the retinal ganglion cells were lost at 14 days after the insult. The number of cells in the inner nuclear layer and the thickness of the inner plexiform layers were also signifcantly decreased. In the GluR ε 1 knockout mice, however, the extent of cell degeneration was lower than in the wild type under the same ischemic condition. In contrast, in the GluR ε 2 knockout mice, no cell degeneration was observed by day 3, but after day 7, they presented severe degeneration as that seen in the wild type. These results suggest that the NMDA recepter channel subunits, especially GluR ε 1 subunit, may have a direct role in the mechanism of retinal neuronal cell death.},
 pages = {445--455},
 title = {一過性虚血による遅発性網膜神経細胞死におけるNMDA型受容体の役割},
 volume = {116},
 year = {2002}
}