Supported by Grants AA10158 (GSW), AA12837 (MEM), AA12839 (DFW), and GCRC (NIH/NCRR M01RR00052).
Striatal Dopamine Release and Family History of Alcoholism
Article first published online: 1 JUN 2006
Alcoholism: Clinical and Experimental Research
Volume 30, Issue 7, pages 1143–1151, July 2006
How to Cite
Munro, C. A., McCaul, M. E., Oswald, L. M., Wong, D. F., Zhou, Y., Brasic, J., Kuwabara, H., Kumar, A., Alexander, M., Ye, W. and Wand, G. S. (2006), Striatal Dopamine Release and Family History of Alcoholism. Alcoholism: Clinical and Experimental Research, 30: 1143–1151. doi: 10.1111/j.1530-0277.2006.00130.x
- Issue published online: 1 JUN 2006
- Article first published online: 1 JUN 2006
- Received for publication October 10, 2005; accepted February 16, 2006.
- Family History;
Background: The offspring of alcohol-dependent individuals are at increased risk for alcoholism. The present study was designed to determine whether mesolimbic dopamine binding potential (BP), dopamine release, stress hormones, and subjective responses to intravenous amphetamine are different in nonalcoholic offspring from families with a history of alcohol dependence [family history positive (FHP)] than in nonalcoholic offspring without a family history of alcohol dependence [family history negative (FHN)].
Methods: Participants were 41 healthy men and women (11 FHP, 30 FHN; age range 18–29). After completing baseline psychiatric symptom and personality measures, striatal D2/D3 dopamine BP and dopamine release in response to an amphetamine challenge were measured with positron emission tomography (PET) using the D2/D3 dopamine (DA) receptor radioligand [11C]raclopride. Binding potential was defined as Bmax/KD, percent change in BP from baseline defined dopamine release. During the scans, subjects rated the degree to which they were experiencing each of 10 possible drug effects. Plasma cortisol and growth hormone (GH) were also measured at scheduled intervals during the scans.
Results: Neither baseline BP nor dopamine release differed by family history. Similarly, subjective responses to amphetamine did not differ by a family history of alcoholism. Although both cortisol and GH increased following administration of amphetamine, these increases did not differ between family history groups.
Conclusions: Using amphetamine to provoke mesolimbic dopamine, we did not show significant differences in dopamine release, subjective responses, or stress hormone measures as a function of family history of alcoholism.