The role of glycine in anoxia aglycaemia-induced potentiation of N-methyl-D-aspartate receptor-mediated postsynaptic potentials in the rat hippocampus

被引：8

作者：

Jones, MG

Szatkowski, MS

机构：

[1] Department of Physiology, St. Mary's Hospital Medical School, Imperial College, London, W2 1PG, Norfolk Place

来源：

NEUROSCIENCE LETTERS | 1995年 / 201卷 / 03期

基金：

英国惠康基金;

关键词：

ischaemia; glutamate; synaptic plasticity; N-methyl-D-aspartate receptor; hippocampus; glycine;

D O I：

10.1016/0304-3940(95)12174-9

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

During brain ischaemia there is a sustained increase in extracellular glycine levels, and the potential role of these changes in modulating N-methyl-D-aspartate (NMDA) receptor-mediated activity following an anoxic/aglycaemic insult was studied in the rat hippocampal slice. Addition of large saturating concentrations of glycine (100 mu M and 1 mM) to the superfusate resulted in increased extracellularly recorded NMDA receptor-mediated components of excitatory postsynaptic potentials (EPSPs) recorded in area CA1. The effects of added glycine were strychnine-insensitive and blocked by a competitive NMDA antagonist. Anoxic/aglycaemic insults to the tissue caused persistent increases in NMDA receptor-mediated EPSPs, but the magnitude of the observed upregulation was unaffected by the presence of added saturating concentrations of glycine. The data suggests that alterations in glycine levels after oxygen deprivation are not responsible for the long term modulation of NMDA receptor activity.

引用

页码：227 / 230

页数：4

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