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   <subfield code="a">Alcohol withdrawal reaction as a result of adaptive changes of excitatory amino acid receptors</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Göran Engberg, Mihály Hajós]</subfield>
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   <subfield code="a">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.</subfield>
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   <subfield code="a">Springer-Verlag, 1992</subfield>
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   <subfield code="a">Locus coeruleus</subfield>
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