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Voluntary ethanol intake increases extracellular acetylcholine levels in the ventral tegmental area in the rat.

Journal article
Authors Anna Larsson
Lena Edström
Lennart Svensson
Bo Söderpalm
Jörgen Engel
Published in Alcohol and Alcoholism
Volume 40
Issue 5
Pages 349-358
Publication year 2005
Published at Institute of Physiology and Pharmacology, Dept of Pharmacology
Institute of Clinical Neurosciences, Section of Psychiatry
Pages 349-358
Language en
Keywords ethanol, ventral tegmental area, acetylcholine, nucleus accumbens, dopamine, in vivo microdialysis, mice
Subject categories Physiology


AIMS: Concurrent use of ethanol and nicotine (tobacco) is often seen in human beings. In previous animal experiments, we have demonstrated that nicotinic acetylcholine receptors, especially alpha-conotoxin MII and mecamylamine sensitive receptors located in the ventral tegmental area may be involved in the stimulatory, dopamine enhancing, and rewarding effects of ethanol in rodents. Ethanol may exert these effects via direct interaction with nicotinic acetylcholine receptors and/or indirectly via enhancement of extracellular acetylcholine levels in the ventral tegmental area. The present experiments investigated a possible indirect effect of ethanol in stimulating the mesoaccumbal dopamine system. METHODS: Neurochemical effects of voluntary ethanol intake on extracellular ventral tegmental acetylcholine and accumbal dopamine levels were measured by means of in vivo microdialysis with a two-probe approach in freely moving rats. RESULTS: Obtained data indicate that voluntary ethanol intake ( approximately 0.7 g/kg/h) leads to an increase of extracellular acetylcholine levels in the ventral tegmental area, and an almost time-locked increase of dopamine levels in the nucleus accumbens. A positive correlation between the ventral tegmental acetylcholine levels and ethanol intake as well as preference was also observed. CONCLUSION: The present results suggest that voluntary ethanol intake enhances extracellular ventral tegmental acetylcholine that may interact with nicotinic acetylcholine receptors, possibly alpha-conotoxin MII sensitive receptors, localized in the ventral tegmental area that subsequently may stimulate dopamine overflow in the nucleus accumbens.

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