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Ethanol-induced dopamine elevation in the rat--modulatory effects by subchronic treatment with nicotinic drugs.

Journal article
Authors Elin Löf
Pei Pei Chau
Rosita Stomberg
Bo Söderpalm
Published in European journal of pharmacology
Volume 555
Issue 2-3
Pages 139-47
ISSN 0014-2999
Publication year 2007
Published at Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Institute of Neuroscience and Physiology, Department of Pharmacology
Pages 139-47
Language en
Keywords Animals, Central Nervous System Depressants, pharmacokinetics, pharmacology, Corpus Striatum, drug effects, metabolism, Diazepam, pharmacology, Dopamine, biosynthesis, Ethanol, pharmacokinetics, pharmacology, GABA Modulators, pharmacology, Hexamethonium, pharmacology, Male, Nicotine, pharmacology, Nicotinic Agonists, pharmacology, Nicotinic Antagonists, pharmacology, Nucleus Accumbens, drug effects, metabolism, Rats, Rats, Wistar, Receptors, GABA, metabolism
Subject categories Pharmacology, Biological research on drug dependence, Neurobiology, Substance Abuse


Chronic nicotine administration is associated with increased ethanol consumption in laboratory animals and in humans. Some smokers report less sedation during acute ethanol intoxication after nicotine administration and the sedative effects from ethanol are mediated by inhibitory GABA(A)-receptors. In a series of in vivo microdialysis experiments we investigated whether subchronic pre-treatment with nicotinic drugs known to enhance ethanol consumption in the rat (nicotine or the peripheral nicotinic antagonist hexamethonium) could modulate the alterations in extracellular dopamine observed in response to administration of ethanol or the sedative GABA(A)-agonist diazepam. In the nucleus accumbens and the dorsal striatum, systemic and/or local ethanol administration resulted in transient increases in extracellular dopamine levels that returned to baseline before the local levels of ethanol started to decline. In hexamethonium pre-treated rats, however, the nucleus accumbens dopamine levels were time-locked to the ethanol levels in the same area after systemic or local ethanol administration. Perfusion of diazepam into the nucleus accumbens produced a significant reduction in nucleus accumbens dopamine in controls. Prior subchronic treatment with nicotine or hexamethonium abolished this effect. The present results suggest that subchronic treatment with the nicotinic acetylcholine receptor antagonist hexamethonium reduces a GABA(A)-R mediated counteraction of the nucleus accumbens dopamine response to ethanol. Additionally, we demonstrate that modulation of nicotinic receptors may reduce the sensitivity of GABA(A) receptors to benzodiazepines. These phenomena may offer a novel explanation to why nicotine and alcohol are often co-abused.

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