1Department of Forensic Psychiatry, Niuvanniemi Hospital, University of Kuopio, FIN-70240 Kuopio, Finland
2Department of Pharmacology and Toxicology, University of Kuopio, PO Box 1627, FIN-70211 Kuopio, Finland
3Department of Clinical Neuroscience, Psychiatry Section, Karolinska Institute and Hospital, S-17176 Stockholm, Sweden
4Department of Clinical Physiology and Nuclear Medicine, Kuopio University Hospital, PO Box 1777, FIN-70211 Kuopio, Finland
5Department of Forensic Medicine, University of Oulu, Kajaanintie 52 D, FIN-90220, Oulu, Finland
6Department of Psychiatry, University of Oulu, Peltolantie 5, FIN-90210, Oulu, Finland
7Department of Pharmaceutical Chemistry, University of Kuopio, PO Box 1627, FIN-70211 Kuopio, Finland
8MAP-Medical Technologies Oy, PO Box 9, FIN-00251 Helsinki, Finland
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Alcohol acts through mechanisms involving the brain neurotransmitter dopamine (DA) with the nucleus accumbens as the key zone for mediating these effects. We evaluated the densities of DA D2/D3 receptors and transporters in the nucleus accumbens and amygdala of post-mortem human brains by using [125l]epidepride and [125I]PE2I as radioligands in whole hemispheric autoradiography of Cloninger type 1 and 2 alcoholics and healthy controls. When compared with controls, the mean binding of [125I]epidepride to DA D2/D3 receptors was 20% lower in the nucleus accumbens and 41% lower in the amygdala, and [125I]PE2I binding to DA transporters in the nucleus accumbens was 39% lower in type 1 alcoholics. These data indicate that dopaminergic functions in these limbic areas may be impaired among type 1 alcoholics, due to the substantially lower number of receptor sites. Our results suggest that such a reduction may result in the chronic overuse of alcohol as an attempt to stimulate DA function. Molecular Psychiatry (2001) 6, 261-267. |
