A GLYCINE ANTAGONIST REDUCES ISCHEMIA-INDUCED CA1 CELL LOSS INVIVO

被引：31

作者：

WOOD, ER ^{[1
]}

BUSSEY, TJ ^{[1
]}

PHILLIPS, AG ^{[1
]}

机构：

[1] UNIV BRITISH COLUMBIA,DEPT PSYCHOL,2136 W MALL,VANCOUVER V6T 1Z4,BC,CANADA

来源：

NEUROSCIENCE LETTERS | 1992年 / 145卷 / 01期

基金：

加拿大自然科学与工程研究理事会;

关键词：

ISCHEMIA; GLYCINE; GLUTAMATE; N-METHYL-D-ASPARTATE RECEPTOR; EXCITOTOXICITY;

D O I：

10.1016/0304-3940(92)90191-9

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Excessive activation of the N-methyl-D-aspartate (NMDA) receptor-channel complex has been implicated as one of the mechanisms by which ischemia-induced neuronal damage is mediated. Elevated glycine levels during ischemia may contribute to damage mediated by the NMDA receptor as glycine binding potentiates NMDA responses, and may be necessary for channel opening. We investigated the protective effects of 7-chlorokynurenic acid - a competitive antagonist at the glycine binding site associated with the NMDA receptor - against hippocampal CA1 cell loss induced by transient forebrain ischemia in rats. Intraventricular administration of the drug immediately before the onset of ischemia significantly attenuated neuronal loss compared to vehicle-treated animals.

引用

页码：10 / 14

页数：5

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