CALCIUM-DEPENDENT COMPONENT OF MASSIVE INCREASE IN EXTRACELLULAR POTASSIUM DURING CEREBRAL-ISCHEMIA AS DEMONSTRATED BY MICRODIALYSIS INVIVO

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 Ca2+-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, Ca2+-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 Ca2+-dependent exocytotic release of neurotransmitters from depolarized nerve terminals.