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Alcohol and Alcoholism Advance Access published online on May 16, 2005
Alcohol and Alcoholism, doi:10.1093/alcalc/agh163
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© The Author 2005. Published by Oxford University Press on behalf of the Medical Council on Alcohol. All rights reserved
Received February 3, 2004
Revised November 16, 2004
Accepted November 16, 2004

Article

EFFECTS OF NALTREXONE ON THE ETHANOL-INDUCED CHANGES IN THE RAT CENTRAL DOPAMINERGIC SYSTEM

YONG-KYU LEE 1, SUNG-WOO PARK 2, YOUNG-KYUNG KIM 2, DAI-JIN KIM 3, JAESEUNG JEONG 4, HUGH MYRICK 5, and YOUNG-HOON KIM 2*

1 Department of Food and Biotechnology, Dongseo University, Busan, South Korea
2 Department of Neuropsychiatry, School of Medicine, Paik Institute for Clinical Research, Inje University, Busan, South Korea
3 Department of Psychiatry, College of Medicine, The Catholic University of Korea, Seoul, South Korea
4 Department of BioSystems, Korea Advanced Institute of Science and Technology, Daejeon 305-701, South Korea
5 Department of Psychiatry, Medical University of South Carolina, SC, USA

* To whom correspondence should be addressed.
YOUNG-HOON KIM, E-mail: npkyh{at}chol.com


  Abstract

Aims: The opioid antagonist naltrexone may reduce ethanol reward, but the underlying neurochemical mechanisms has yet to be clarified. The afferent projections to the nucleus accumbens from the ventral tegmental area (VTA) provide a potential substrate by which endogenous opioids may modulate the dopaminergic rewarding effects of ethanol. We assessed mRNA levels of tyrosine hydroxylase (TH), a major regulatory enzyme in the dopamine synthesis and levels of dopamine and its metabolites after chronic ethanol administration with and without concomitant naltrexone. Methods: Sprague-Dawley rats were exposed to chronic ethanol consumption (5%, 4 weeks) with and without concomitant naltrexone administration. Levels of TH mRNA in the VTA and substantia nigra (SN) and dopamine and its metabolites in the striatum of the rats were measured by in situ hybridization and by high performance liquid chromatography, respectively. Results: Chronic ethanol consumption increased TH mRNA levels in the VTA, but did not cause any significant change in the SN. With naltrexone treatment, ethanol-induced increase in the TH mRNA level was reduced in the VTA. Chronic ethanol consumption did not cause any change in the levels of dopamine and its metabolites in most brain regions. Only in the striatum, ethanol consumption with naltrexone treatment significantly increases the dopamine level. Conclusion: This finding supports the presence of interactions of opioid and dopaminergic systems in the VTA in mediating ethanol reward, and thus naltrexone attenuates the rewarding properties of ethanol by interfering with the ethanol-induced stimulation of the mesolimbic dopaminergic pathway.


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