Inhibition of rapid potassium flux during cerebral ischemia in vivo with an excitatory amino acid antagonist.
Previous studies have demonstrated that microdialysis is capable of detecting an abrupt and massive increase in extracellular K+ concentration ([K+]e) and a concomitant increase in extracellular concentration of excitatory amino acids (EAAs) during cerebral ischemia in the rat hippocampus in vivo. Following in situ administration of kynurenic acid (KYN), a broad-spectrum antagonist of EAAs, through the dialysis probe (5-10 mM), a delay in reaching the maximum level of increased [K+]e was observed in a dose-dependent manner. The initial component of the rapid increase in [K+]e appears to be mediated by EAAs released from nerve terminals.
Katayama
Y
Y
Division of Neurosurgery, University of California, School of Medicine, Los Angeles 90024.
Tamura
T
T
Becker
D P
DP
Tsubokawa
T
T
D000596:Amino Acids / Q000037:antagonists & inhibitors; D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism*; D003956:Dialysis / Q000379:methods; D005260:Female; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism*; D007700:Kinetics; D007736:Kynurenic Acid / Q000494:pharmacology*; D018377:Neurotransmitter Agents / Q000037:antagonists & inhibitors; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors
D000596:Amino Acids; D018377:Neurotransmitter Agents; D007736:Kynurenic Acid; D011188:Potassium