Katayama Y, Kawamata T, Tamura T, Hovda D A, Becker D P, Tsubokawa T
Division of Neurosurgery, UCLA School of Medicine, University of California, Los Angeles 90024.
Brain Res. 1991 Aug 30;558(1):136-40. doi: 10.1016/0006-8993(91)90730-j.
The changes in extracellular glutamate ([Glu]e) and potassium ([K+]e) in the rat hippocampus during cerebral ischemia were determined simultaneously by microdialysis in vivo. Biphasic increases in [Glu]e, i.e. an earlier rapid increase concomitant with an abrupt increase in [K+]e followed by a later slow increase, were observed. Dialysis with Ca(2+)-free perfusate containing Co2+ blocked the earlier rapid increase completely but the later slow increase only partially. These findings suggest that Ca(2+)-dependent exocytotic release from the presynaptic nerve terminals is involved predominantly in the earlier rapid increase in [Glu]d. The later slow increase in [Glu]d may be due in part to a breakdown of membrane function resulting from several causes, including a loss of the electrogenic component of the glutamate gradients across the plasma membrane, and a loss of function of the glutamate uptake system.
通过体内微透析同时测定大鼠脑缺血期间海马细胞外谷氨酸（[Glu]e）和钾（[K+]e）的变化。观察到[Glu]e呈双相增加，即早期快速增加伴随着[K+]e的突然增加，随后是后期缓慢增加。用含Co2+的无Ca(2+)灌流液透析可完全阻断早期快速增加，但仅部分阻断后期缓慢增加。这些发现表明，突触前神经末梢的Ca(2+)依赖性胞吐释放主要参与了[Glu]d的早期快速增加。[Glu]d的后期缓慢增加可能部分归因于多种原因导致的膜功能破坏，包括跨质膜的谷氨酸梯度的电生成分丧失以及谷氨酸摄取系统功能丧失。
