@article{oai:kumadai.repo.nii.ac.jp:00021867,
 author = {浜, 康博 and 香月, 博志 and 栃川, 宣永 and 角中, ちひろ and 久米, 利明 and 赤池, 昭紀 and Hama, Yasuhiro and 香月, 博志 and Katsuki, Hiroshi and Tochikawa, Yoshinaga and Suminaka, Chihiro and 久米, 利明 and Kume, Toshiaki and 赤池, 昭紀 and Akaike, Akinori},
 issue = {3},
 journal = {Neuroscience Research},
 month = {Nov},
 note = {application/pdf, 論文(Article), N-Methyl-d-aspartate (NMDA) receptors, which play an important role in neuronal excitotoxicity, require not only agonists at the glutamate-binding site but also co-agonists at the glycine site for their activation. Here we examined the role of endogenous agonists at the glycine site of NMDA receptors in excitotoxic retinal damage in vivo. To quantify the number of surviving retinal ganglion cells (RGCs), we injected a retrograde tracer, fluoro-gold, into the superior colliculus bilaterally and subsequently counted RGCs on whole-mounted retinas. Co-injection of 5,7-dichlorokynurenic acid (300 nmol), a competitive antagonist at the glycine site of NMDA receptors, rescued RGCs from damage induced by 200 nmol NMDA. On the other hand, RGC death induced by 20 nmol NMDA was enhanced by addition of glycine (10 nmol), d-serine (10 nmol) or a competitive glycine transporter-1 inhibitor, sarcosine (0.3 or 3 nmol). Moreover, application of d-serine-degrading enzyme, d-amino acid oxidase (30 mU), partially suppressed RGC death induced by 20 nmol NMDA. These results suggest that the severity of excitotoxic retinal damage in vivo depends on the levels of both glycine and d-serine., http://www.elsevier.com/wps/find/journaldescription.cws_home/506082/description#description},
 pages = {279--285},
 title = {Contribution of endogenous glycine site NMDA agonists to excitotoxic retinal damage in vivo},
 volume = {56},
 year = {2006},
 yomi = {カツキ, ヒロシ and クメ, トシアキ and アカイケ, アキノリ}
}