Inhibition of the high-affinity glutamate uptake system facilitates the massive potassium flux during cerebral ischaemia in vivo
- 1 April 1995
- journal article
- research article
- Published by Taylor & Francis in Neurological Research
- Vol. 17 (2) , 94-96
- https://doi.org/10.1080/01616412.1995.11740294
Abstract
During cerebral ischaemia, the extracellular concentration of K+ ([K+d]e) increases abruptly to 50-60 mM following an initial slow increase to 6-70 mw. We have recently shown that the increase in [K+]e is significantly delayed by in situ administration of kynurenic acid, a broad spectrum antagonist of excitatory amino acids, suggesting that the catastrophic ionic fluxes occurring during ischaemia are initially mediated by EAA-coupled ion channels. In order to confirm further the role of EAAs, the changes in extracellular K+ (IK+]e) and glutamate ([Clu]J during cerebral ischaemia were determined in the rat hippocampus by microdialysis in vivo, and the effect of dihydrokainate (DHKA), an inhibitor of the high-affinity uptake system of EAAs; was examined by in situ administration through the dialysis probe. DHKA induced a significant increase in baseline [Glu]e and facilitated the abrupt increase in [K+]e during cerebral ischaemia. These findings support the hypothesis that EAAs play a vital role in producing the rapid ionic shifts earlier during cerebral ischaemia. [Neurol Res 1995; 17: 94–96]Keywords
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