Naunyn-Schmiedeberg's Archives of Pharmacology

, Volume 340, Issue 5, pp 516–521

Inhibition of N-methyl-d-aspartate (NMDA) and l-glutamate-induced noradrenaline and acetylcholine release in the rat brain by ethanol

  • M. Göthert
  • K. Fink

DOI: 10.1007/BF00260606

Cite this article as:
Göthert, M. & Fink, K. Naunyn-Schmiedeberg's Arch Pharmacol (1989) 340: 516. doi:10.1007/BF00260606


The influence of ethanol on stimulation-evoked 3H-transmitter release was examined in slices of the rat brain cortex and corpus striatum preincubated with 3H-noradrenaline and 3H-choline, respectively. 3H-Transmitter release was stimulated by NMDA, l-glutamate, electrical impulses, reintroduction of Ca2+ ions (“Ca2+-evoked release”; after superfusion with Ca2+-free, K+-rich solution) or veratridine. In cortical slices preincubated with 3H-noradrenaline and superfused with Mg2+-free, otherwise physiologically composed salt solution, ethanol inhibited the NMDA- or l-glutamate-induced tritium overflow (IC50 45 and 37 mmol/l, respectively). In contrast, the tritium overflow in response to electrical stimulation, reintroduction of Ca2+ ions or veratridine was not affected by ethanol at concentrations up to 320 mmol/l; these experiments were carried out in cortical slices superfused with solution containing a physiological Mg2+ concentration. Ethanol also failed to inhibit Ca2+-evoked release in the absence of Mg2+ ions. In the presence of 1 μmol/l veratridine, but not in its absence, NMDA induced tritium overflow even when cortical slices were superfused with salt solution containing a physiological Mg2+ concentration; again, ethanol inhibited this NMDA-evoked tritium overflow (IC50 73 mmol/l). In striatal slices preincubated with 3H-choline and superfused with Mg2+-free “physiological” salt solution, the NMDA-evoked tritium overflow was also, although at lower potency, inhibited by ethanol (IC50 192 mmol/l).

In spite of the differences between the IC50 values of ethanol determined for the inhibition of cortical noradrenaline and striatal acetylcholine release, it may be concluded that the NMDA receptor-ion channel complex is one of the sites of action underlying the ethanol-induced inhibition of neurotransmitter release. Since in the brain cortex the NMDA-induced 3H-noradrenaline release appears to be mediated by an excitatory interneurone activated by NMDA, this neuronal system may be involved in the cortical actions of ethanol.

Key words

EthanolNMDA receptorNoradrenaline releaseAcetylcholine releasel-glutamate

Copyright information

© Springer-Verlag 1989

Authors and Affiliations

  • M. Göthert
    • 1
  • K. Fink
    • 1
  1. 1.Institut für Pharmakologie und Toxikologie der Rheinischen Friedrich-Wilhelms-Universität BonnBonn 1Germany