Calcium-dependent component of massive increase in extracellular potassium during cerebral ischemia as demonstrated by microdialysis in vivo.
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.
Katayama
Y
Y
Division of Neurosurgery, UCLA School of Medicine 90024.
Tamura
T
T
Becker
D P
DP
Tsubokawa
T
T
D000818:Animals; D001921:Brain / Q000378:metabolism*; D002545:Brain Ischemia / Q000378:metabolism*; D002118:Calcium / Q000494:pharmacology*; D003035:Cobalt / Q000494:pharmacology; D003956:Dialysis; D005110:Extracellular Space / Q000187:drug effects / Q000378:metabolism; D007700:Kinetics; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D003035:Cobalt; D011188:Potassium; D002118:Calcium