Abstract # 13378 Poster # 152:

Scheduled for Friday, August 23, 2019 06:00 PM-08:00 PM: (Alumni Lounge) Poster Presentation


CENTRAL NERVOUS SYSTEM MONOAMINE RESPONSE TO ALCOHOL IS ASSOCIATED WITH FUTURE ALCOHOL CONSUMPTION IN LABORATORY-HOUSED RHESUS MACAQUES (MACACA MULATTA)

E. K. Wood1, D. P. Lemmon1, N. D. Mullen1, S. G. Lindell2,3, M. L. Schwandt3, C. S. Barr2,3 and S. J. Suomi4
1Psychology Department, Brigham Young University, Provo, UT 84062, Brigham Young University, 1001 KMBL, Provo, Utah 84602, USA, 2Section of Comparative Behavioral Genomics, National Institute on Alcohol Abuse and Alcoholism, NIH, Rockville, MD 20852, 3Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD 20892, 4Section of Comparative Ethology, Eunice Shriver Kennedy National Institute of Child Health and Human Development, NIH, Poolesville, MD 20837
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     Impaired monoamine neurotransmission is widely held to increase the risk for alcohol abuse and to play a role in tolerance to alcohol. Few studies, however, have directly assessed this. This research assesses the relationship of central monoamine response following first-time alcohol exposure and subsequent alcohol consumption using a nonhuman primate model. As early parental absence modulates both central monoamine development and adolescent alcohol intake, alcohol-induced monoamine metabolite changes as they lead to alcohol intake in mother- and peer-reared subjects are also examined. N=114 adolescent, alcohol-naïve rhesus macaques were administered an intravenous bolus of 16.8% alcohol solution on two occasions, one month apart. Prior to and one hour following each infusion, cerebrospinal fluid (CSF) was obtained and assayed for monoamine metabolite concentrations. Eight months later, subjects were given access to a sweetened, 8.4% alcohol solution for one hour per day, over one month. Paralleling other studies, peer-reared subjects consumed significantly more alcohol than did mother-reared subjects (p<0.002). Controlling for rearing, results showed that CSF monoamine metabolite concentrations were individually trait-like, exhibiting positive correlations between baseline and post-infusion (p<0.00001). Monoamine metabolites showed robust increases in response to alcohol infusion, with subjects that showed low baseline and low changes from baseline consuming the most alcohol (p<0.02). These findings suggest that low baseline and central monoamine response to alcohol are important factors in the risk for excessive alcohol consumption.