Ikeda M, Nakazawa T, Abe K, Kaneko T, Yamatsu K
Tsukuba Research Laboratories, Eisai Co., Ltd., Ibaraki, Japan.
Neurosci Lett. 1989 Jan 16;96(2):202-6. doi: 10.1016/0304-3940(89)90058-x.
Calcium dependency of ischemia-induced increase in extracellular glutamate in the hippocampus was studied in vitro and in vivo. Perfusion of a low pO2 medium without glucose (in vitro ischemia) induced an increase in extracellular glutamate in rat hippocampal slices. This increase did not depend on Ca2+, which is in contrast with the observation that about 40% of membrane depolarization (50 mM KCl)-evoked release was Ca2+-dependent. In vivo cerebral ischemia of 5 min duration in gerbils also caused Ca2+-independent increase in extracellular glutamate in the hippocampus. The data suggest that the increase in extracellular glutamate induced by ischemia is not due to the enhanced release of neurotransmitter glutamate.
在体外和体内研究了海马体中缺血诱导的细胞外谷氨酸增加对钙的依赖性。灌注不含葡萄糖的低氧分压培养基（体外缺血）可诱导大鼠海马切片中细胞外谷氨酸增加。这种增加不依赖于Ca2+，这与以下观察结果形成对比：约40%的膜去极化（50 mM KCl）诱发的释放是Ca2+依赖性的。在沙土鼠体内进行5分钟的脑缺血也会导致海马体中细胞外谷氨酸的增加且不依赖于Ca2+。数据表明，缺血诱导的细胞外谷氨酸增加并非由于神经递质谷氨酸的释放增强所致。
