Katayama Y, Tamura T, Becker D P, Tsubokawa T
Division of Neurosurgery, UCLA School of Medicine 90024.
Brain Res. 1991 Dec 13;567(1):57-63. doi: 10.1016/0006-8993(91)91435-4.
This study characterizes the physiological features and limitations of K(+)-free dialysis to detect changes in extracellular concentration of K+ ([K+]e) in the rat hippocampus in vivo. It also demonstrates the effects of Ca(2+)-free perfusate containing Co2+ or Mg2+, which blocks Ca2+ entry into the presynaptic nerve terminal, on the abrupt increase in [K+]e detected by this technique during cerebral ischemia. K(+)-free dialysis for 40 min caused no significant changes in the baseline [K+]e. In contrast, Ca(2+)-free dialysis for 40 min significantly reduced the extracellular Ca2+ concentration. Under this condition, together with addition of Co2+ or Mg2+ to the perfusate, the increase in [K+]e was delayed, and a delay in reaching the maximum level was observed in a dose-dependent manner. These results are consistent with the hypothesis that the initial increase in [K+]e during cerebral ischemia is related to the Ca(2+)-dependent exocytotic release of neurotransmitters from depolarized nerve terminals.
本研究描述了无钾透析在体内检测大鼠海马体中细胞外钾离子浓度（[K⁺]e）变化时的生理特征和局限性。同时还证明了含Co²⁺或Mg²⁺的无钙灌注液对该技术检测到的脑缺血期间[K⁺]e突然升高的影响，这种无钙灌注液会阻止Ca²⁺进入突触前神经末梢。无钾透析40分钟不会使基线[K⁺]e发生显著变化。相反，无钙透析40分钟会显著降低细胞外Ca²⁺浓度。在此条件下，向灌注液中添加Co²⁺或Mg²⁺后，[K⁺]e的升高会延迟，并且观察到达到最大水平的延迟呈剂量依赖性。这些结果与以下假设一致，即脑缺血期间[K⁺]e的初始升高与去极化神经末梢中神经递质的Ca²⁺依赖性胞吐释放有关。
