Inhibition of rapid potassium flux during cerebral ischemia in vivo with an excitatory amino acid antagonist

Abstract

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.