HOME   English    

Kumamoto University Repository System >
薬学 >
発表論文(薬学系) >



ファイル 記述 サイズフォーマット
Neu Res0056-0279.pdf298KbAdobe PDF見る/開く
タイトル :Contribution of endogenous glycine site NMDA agonists to excitotoxic retinal damage in vivo
著者 :Hama, Yasuhiro
Katsuki, Hiroshi
Tochikawa, Yoshinaga
Suminaka, Chihiro
Kume, Toshiaki
Akaike, Akinori
刊行年月日 :2006-11
収録雑誌名 :Neuroscience Research
巻 :56
号 :3
開始ページ :279
終了ページ :285
要約(Abstract) :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.
URL :http://www.elsevier.com/wps/find/journaldescription.cws_home/506082/description#description
収録種別 :雑誌掲載論文
ISSN :01680102
出版社(者) :Elsevier Ireland Ltd
権利(Rights) :© 2006 Elsevier Ireland Ltd and the Japan Neuroscience Society All rights reserved.
備考 :平成18~19年度科学研究費補助金(基盤研究(C))研究成果報告書 課題番号:18590052『ミクログリアの活性化を介する黒質線条体系ニューロン変性の機序とその防御』pp.65-71に掲載
URI :http://hdl.handle.net/2298/10010
関連 :http://hdl.handle.net/2298/9868
このアイテムの引用には次の識別子を使用してください: http://hdl.handle.net/2298/10010