Calcium-dependent component of massive increase in extracellular potassium during cerebral ischemia as demonstrated by microdialysis in vivo

Abstract

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 Co 2+ or Mg 2+, which blocks Ca 2+ 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 Ca 2+ concentration. Under this condition, together with addition of Co 2+ or Mg 2+ 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.