Laboratory of Clinical Studies, Primate Unit, Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, Poolesville, Maryland 20837-0529, USA
Address for correspondence: Christina S. Barr, V.M.D., Ph.D., Research Fellow, NIH Animal Center, Building 112, P.O. Box 529, Poolesville, MD 20837-0529. Voice: 301-496-9550; fax: 301-435-9278. cbarr{at}mail.nih.gov
Traits characteristic of type I and type II alcoholism are thought
to relate to dysregulated central nervous system serotonin functioning.
In this review, we discuss variables associated with high adolescent
alcohol consumption and other risk-taking behaviors in a nonhuman
primate model. Adolescent primates with low CSF concentrations
of the serotonin metabolite 5-HIAA are more impulsive and exhibit
increased levels of alcohol consumption. Both genetic and environmental
factors contribute to alcohol-seeking behavior in adolescent
macaques. Sequence variation within serotonin system genes,
for example, a repeat polymorphism in the transcriptional control
region of the monoamine oxidase gene (
MAOA-LPR), increases the
propensity for adolescent males to consume alcohol. Environmental
factors, such as early life stress in the form of peer-rearing
or early age of exposure to alcohol, are also associated with
increased alcohol consumption. Peer-reared females, especially
those exposed to alcohol during early adolescence, exhibit increased
rates of alcohol consumption compared to those exposed to alcohol
later in development. When genetic variables are also considered,
there is an interaction between the low activity serotonin transporter
gene promoter
s allele (rh5-HTTLPR) and rearing condition on
alcohol preference in females but not males, suggesting that
the interactions between genes and the environment may be sexually
dichotomous. By learning more about the interactions between
genes, early experience, and alcohol intake in the adolescent
nonhuman primate, we may be able to identify factors that contribute
to the susceptibility, pathogenesis, and progression of impulse
control disorders, such as alcoholism.
