使用兴奋性氨基酸拮抗剂在体内抑制脑缺血期间快速钾离子通量。

Inhibition of rapid potassium flux during cerebral ischemia in vivo with an excitatory amino acid antagonist.

作者信息

Katayama Y, Tamura T, Becker D P, Tsubokawa T

机构信息

Division of Neurosurgery, University of California, School of Medicine, Los Angeles 90024.

出版信息

Brain Res. 1991 Dec 24;568(1-2):294-8. doi: 10.1016/0006-8993(91)91412-t.

DOI:10.1016/0006-8993(91)91412-t

Abstract

Previous studies have demonstrated that microdialysis is capable of detecting an abrupt and massive increase in extracellular K+ concentration ([K+]e) and a concomitant increase in extracellular concentration of excitatory amino acids (EAAs) during cerebral ischemia in the rat hippocampus in vivo. Following in situ administration of kynurenic acid (KYN), a broad-spectrum antagonist of EAAs, through the dialysis probe (5-10 mM), a delay in reaching the maximum level of increased [K+]e was observed in a dose-dependent manner. The initial component of the rapid increase in [K+]e appears to be mediated by EAAs released from nerve terminals.

摘要

先前的研究表明，在大鼠海马体脑缺血的体内实验中，微透析能够检测到细胞外钾离子浓度（[K+]e）的突然大幅升高以及兴奋性氨基酸（EAA）细胞外浓度的相应增加。通过透析探针原位给予EAA的广谱拮抗剂犬尿氨酸（KYN）（5-10 mM）后，观察到[K+]e升高达到最大水平的延迟呈剂量依赖性。[K+]e快速升高的初始成分似乎是由神经末梢释放的EAA介导的。

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