Abstract # 2193 Event # 113:

Scheduled for Friday, June 22, 2007 02:45 PM-03:00 PM: Session 12 (North Main Hall E) Oral Presentation

Gene-environment Interaction Predicts Peripheral Serotonin Transporter Gene Expression in Infant Rhesus Macaques (Macaca mulatta)

E. L. Kinnally1,2, L. A. Lyons2 and J. P. Capitanio1,2
1University of California Davis, Department of Psychology, One Shields Avenue, Davis, CA 95616, USA, 2California National Primate Research Center
     Gene-environment interactions have been shown to shape neurobehavioral development in humans and rhesus macaques. In particular, adverse early experiences and possession of one or two short alleles of the serotonin transporter promoter polymorphism (rh5-HTTLPR) is associated with reduced neural serotonin function, enhanced neural reactivity to fearful stimuli, and reduced behavioral inhibition in adults as well as infants. The mechanism of rh5-HTTLPR genotype-environment interactions is unknown. We tested the hypothesis that gene-environment interactions occur via alterations in gene regulation in infant rhesus macaques. Subjects included 58 infant rhesus macaques reared in one of two conditions: mother reared individuals (MR) were reared in large outdoor enclosures (field cages) with mothers and extended social groups, and nursery reared individuals (NR) had been separated from their mothers early in life and lived in indoor paired-housing. All infants were genotyped for rh5-HTTLPR. We measured serotonin transporter (5-HTT) expression in lymphocytes using quantitative real-time PCR. 5-HTT expression was quantified 2.5 hours following and again 8 hours following removal from social housing. MR infants significantly upregulated 5-HTT gene expression during separation [repeated measures ANOVA and t-tests, a=0.05], while NR infants did not. Further, of MR infants, only "long/long" rh5-HTTLPR homozygotes significantly upregulated 5-HTT during this period. We conclude that gene-environment interactions influencing neurobehavioral development begin at the molecular level, shaping the ability of the individual to regulate 5-HTT response to a stressor.