Alcohol and Alcoholism Advance Access originally published online on July 25, 2005
Alcohol and Alcoholism 2005 40(5):349-358; doi:10.1093/alcalc/agh180
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VOLUNTARY ETHANOL INTAKE INCREASES EXTRACELLULAR ACETYLCHOLINE LEVELS IN THE VENTRAL TEGMENTAL AREA IN THE RAT
Institute of Physiology and Pharmacology, Department of Pharmacology, The Sahlgrenska Academy, Göteborg University, Box 431, SE-405 30 Göteborg, Sweden and 1 Institute of Clinical Neuroscience, Section of Psychiatry, The Sahlgrenska Academy, Göteborg University, SU/Sahlgrenska, SE-413 45 Göteborg, Sweden
* Author to whom correspondence should be addressed at: Tel.: +46 31 773 34 16; Fax: +46 31 773 32 84; E-mail: jorgen.engel{at}pharm.gu.se
(Received 20 April 2005; first review notified 8 May 2005; in revised form 17 May 2005; accepted 19 May 2005)
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 
-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 (
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 -conotoxin MII sensitive receptors, localized in the ventral tegmental area that subsequently may stimulate dopamine overflow in the nucleus accumbens.
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