title: Striatal dopamine release and family history of alcoholism.
abstract: 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.
authors.affiliation: Department of Medicine, The John Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
authors.forename: Cynthia A
authors.initials: CA
authors.lastname: Munro
authors.forename: Mary E
authors.initials: ME
authors.lastname: McCaul
authors.forename: Lynn M
authors.initials: LM
authors.lastname: Oswald
authors.forename: Dean F
authors.initials: DF
authors.lastname: Wong
authors.forename: Yun
authors.initials: Y
authors.lastname: Zhou
authors.forename: James
authors.initials: J
authors.lastname: Brasic
authors.forename: Hiroto
authors.initials: H
authors.lastname: Kuwabara
authors.forename: Anil
authors.initials: A
authors.lastname: Kumar
authors.forename: Mohab
authors.initials: M
authors.lastname: Alexander
authors.forename: Weiguo
authors.initials: W
authors.lastname: Ye
authors.forename: Gary S
authors.initials: GS
authors.lastname: Wand
mesh_terms: D000293:Adolescent; D000328:Adult; D000437:Alcoholism / Q000235:genetics*; D000661:Amphetamine / Q000494:pharmacology; D001479:Basal Ganglia / Q000187:drug effects / Q000378:metabolism*; D004298:Dopamine / Q000378:metabolism*; D005260:Female; D020022:Genetic Predisposition to Disease / Q000523:psychology; D013006:Growth Hormone / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D008297:Male; D049268:Positron-Emission Tomography
chemical_list: D013006:Growth Hormone; D000661:Amphetamine; D004298:Dopamine; D006854:Hydrocortisone