Inhibition of N-methyl-d-aspartate- and kainate-evoked noradrenaline release in human cerebral cortex slices by ethanol |
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Authors: | Klaus Fink Rolf Schultheiß Manfred Göthert |
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Affiliation: | (1) Institute of Pharmacology and Toxicology, University of Bonn, Reuterstrasse 2b, W-5300 Bonn, Federal Republic of Germany;(2) Clinic of Neurosurgery, University of Bonn, Sigmund-Freud-Strasse 25, W-5300 Bonn, Federal Republic of Germany |
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Abstract: | Summary The effect of ethanol on the release of noradrenaline evoked by various stimuli was investigated in human cerebral cortical slices from patients undergoing neurosurgery. The slices were preincubated with [3H]noradrenaline and then superfused. Tritium overflow was stimulated by exposure to N-methyl-d-aspartate (NMDA; in slices superfused without Mg2+), kainic acid, veratridine or by increasing the K+ concentration.The NMDA evoked tritium overflow was concentration-dependently inhibited by ethanol; an inhibition by 37% occurred at 48 mmol/l ethanol. This ethanol concentration was not yet effective when kainic acid was used for stimulation, but ethanol 150 mmol/l strongly inhibited the tritium overflow evoked by kainic acid as well. The tritium overflow evoked by veratridine or high K+ was not affected by ethanol in the concentration range investigated.These findings are compatible with the suggestion that the NMDA receptor and, with less susceptibility, the kainate receptor are sites of action underlying the effect of ethanol in the human brain.Send offprint requests to M. Göthert at the above address |
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Keywords: | Ethanol Human cerebral cortex NMDA receptor Kainate receptor Noradrenaline release |
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