ROLE OF GLYCINE IN THE N-METHYL-D-ASPARTATE-MEDIATED NEURONAL CYTOTOXICITY

被引：115

作者：

PATEL, J

ZINKAND, WC

THOMPSON, C

KEITH, R

SALAMA, A

机构：

[1] Molecular Pharmacology Unit, ICI Pharmaceuticals Group, ICI Americas Inc., Wilmington, Delaware

来源：

JOURNAL OF NEUROCHEMISTRY | 1990年 / 54卷 / 03期

关键词：

Excitatory amino acids; Neurotoxicity; N‐Methyl‐d‐aspartate–Glycine;

D O I：

10.1111/j.1471-4159.1990.tb02329.x

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Abstract: Current evidence indicates that glutamate acting via the N‐methyl‐d‐aspartate (NMDA) receptor/ion channel complex plays a major role in the neuronal degeneration associated with a variety of neurological disorders. In this report the role of glycine in NMDA neurotoxicity was examined. We demonstrate that NMDA‐mediated neurotoxicity is markedly potentiated by glycine and other amino acids, e.g., d‐serine. Putative glycine antagonists HA‐966 and 7‐chlorokynurenic acid were highly effective in preventing NMDA neurotoxicity, even in the absence of added glycine. The neuroprotective action of HA‐966 and 7‐chlorokynurenic acid, but not that of NMDA antagonists 3‐(2‐carboxypiperazine‐4‐yl)propylphosphonate and MK‐801, could be reversed by glycine. These results indicate that glycine, operating through a strychnine‐insensitive glycine site, plays a central permissive role in NMDA‐mediated neurotoxicity. Copyright © 1990, Wiley Blackwell. All rights reserved

引用

页码：849 / 854

页数：6

共 38 条

[1] PHENCYCLIDINE AND GLYCINE MODULATE NMDA-ACTIVATED HIGH CONDUCTANCE CATIONIC CHANNELS BY ACTING AT DIFFERENT SITES [J].