Tupala E, Hall H, Bergström K, Särkioja T, Räsänen P, Mantere T, Callaway J, Hiltunen J, Tiihonen J
Department of Forensic Psychiatry, Niuvanniemi Hospital, University of Kuopio, FIN-70240 Kuopio, Finland.
Mol Psychiatry. 2001 May;6(3):261-7. doi: 10.1038/sj.mp.4000859.
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 D(2)/D(3) receptors and transporters in the nucleus accumbens and amygdala of post-mortem human brains by using [(125)l]epidepride and [(125)I]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 [(125)I]epidepride to DA D(2)/D(3) receptors was 20% lower in the nucleus accumbens and 41% lower in the amygdala, and [(125)I]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.
酒精通过涉及大脑神经递质多巴胺（DA）的机制发挥作用，其中伏隔核是介导这些效应的关键区域。我们使用[¹²⁵I]表螺环哌啶和[¹²⁵I]PE2I作为放射性配体，在克隆宁格1型和2型酗酒者及健康对照者的全脑半球放射自显影中，评估了死后人类大脑伏隔核和杏仁核中DA D(2)/D(3)受体及转运体的密度。与对照组相比，[¹²⁵I]表螺环哌啶与DA D(2)/D(3)受体的平均结合在伏隔核中降低了20%，在杏仁核中降低了41%，并且在1型酗酒者中，[¹²⁵I]PE2I与伏隔核中DA转运体的结合降低了39%。这些数据表明，由于受体位点数量大幅减少，1型酗酒者这些边缘区域的多巴胺能功能可能受损。我们的结果表明，这种减少可能导致长期过度饮酒，试图刺激DA功能。
