부산대학교 도서관

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.biopsych.2005.11.005 Byline: Ahmad R. Hariri (a), Emily M. Drabant (b), Daniel R. Weinberger (b) Keywords: Emotion; mood disorders; serotonin; amygdala; prefrontal cortex; neuroimaging; genetics Abstract: Advances in molecular biology and neuroimaging have provided a unique opportunity to explore the relationships between genes, brain, and behavior. In this review, we will briefly outline the rationale for studying genetic effects on brain function with neuroimaging. We will then use studies of genetically driven variation in serotonin transporter function on corticolimbic structure and function to highlight the effectiveness of this strategy to delineate biological pathways and mechanisms by which individual differences in brain function emerge and potentially bias behavior and risk for psychiatric illness. In a series of studies, a relatively frequent regulatory variant of the human serotonin transporter gene (5-HTTLPR) has been demonstrated to bias the reactivity of the amygdala to salient environmental cues. Moreover, the 5-HTTLPR affects the development of a broader corticolimbic circuit and alters the functional integration of emotional information between the amygdala and medial prefrontal cortex. In turn, corticolimbic circuit function predicts individual differences in an experimental index of temperamental anxiety and, thus, might reflect a predictive biological marker of increased risk for mood disorders associated with the 5-HTTLPR. Author Affiliation: (a) Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania (b) Genetics of Cognition and Psychosis Program, IRP, NIMH/NIH/DHHS, Bethesda, Maryland Article History: Received 10 June 2005; Revised 1 November 2005; Accepted 14 November 2005