Kataoka Y, Koizumi S, Kohzuma M, Shibaguchi H, Shigematsu K, Niwa M, Taniyama K
Department of Pharmacology 2, Nagasaki University School of Medicine, Japan.
Eur J Pharmacol. 1995 Feb 6;273(3):285-9. doi: 10.1016/0014-2999(94)00754-u.
The high K(+)-evoked dopamine release from rat striatal slices remained impaired by 50% up to 2 h after pulse exposure of the tissues to endothelin-3, under conditions of hypoglycemia/hypoxia. This striatal dysfunction was significantly improved by D-2-amino-5-phosphonopentanoic acid, a NMDA receptor antagonist, at a much lower concentration than that providing protection against NMDA-evoked dysfunction. In light of these findings, the important role of glutamatergic mechanisms, especially NMDA receptors, in mediating endothelin neurotoxicity warrants further attention.
在低血糖/低氧条件下，大鼠纹状体切片经内皮素-3脉冲暴露后长达2小时，高钾诱发的多巴胺释放仍受损50%。D-2-氨基-5-磷酸戊酸（一种NMDA受体拮抗剂）能显著改善这种纹状体功能障碍，其浓度远低于提供抗NMDA诱发功能障碍保护作用的浓度。鉴于这些发现，谷氨酸能机制，尤其是NMDA受体，在介导内皮素神经毒性中的重要作用值得进一步关注。
