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Alcohol withdrawal reaction as a result of adaptive changes of excitatory amino acid receptors

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Summary

Recent electrophysiological and biochemical studies suggest that ethanol interferes with excitatory amino acid (EAA) neurotransmission. Here, we present electrophysiological evidence that, following cessation of a chronic ethanol treatment, noradrenergic locus coeruleus (LC) neurons display hyperactivity at the same time as a specifically enhanced sensitivity to microiontophoretically applied NMDA or quisqualate. Furthermore, after chronic ethanol treatment, but not before, the NMDA receptor antagonist MK 801 (0.3–2.4 mg/kg, i.v.) dose-dependently inhibited the firing of the LC neurons. Our data indicate that an up-regulation of EAA receptors located on LC neurons accounts for the changes in LC firing in ethanol-treated rats. We propose that activation of the LC contributes to the clinical signs of the ethanol abstinence reaction and that EAA antagonists may be beneficial therapeutically for its treatment.

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Correspondence to G. Engberg at the above address

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Engberg, G., Hajós, M. Alcohol withdrawal reaction as a result of adaptive changes of excitatory amino acid receptors. Naunyn-Schmiedeberg's Arch Pharmacol 346, 437–441 (1992). https://doi.org/10.1007/BF00171087

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  • DOI: https://doi.org/10.1007/BF00171087

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