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Social Cognitive and Affective Neuroscience Advance Access published online on October 25, 2009
Social Cognitive and Affective Neuroscience, doi:10.1093/scan/nsp035
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© The Author (2009). Published by Oxford University Press. For Permissions, please email: journals.permissions@oxfordjournals.org

Serotonin transporter genotype modulates amygdala activity during mood regulation

Seth J. Gillihan1, Hengyi Rao2,3, Jiongjiong Wang2, John A. Detre2, Jessica Breland1, Geena Mary V. Sankoorikal4, Edward S. Brodkin4 and Martha J. Farah1

1Center for Cognitive Neuroscience, Department of Psychology, 2Center for Functional Neuroimaging, Department of Neurology and Department of Radiology, University of Pennsylvania, Philadelphia, PA 19104, USA, 3Center for Functional Brain Imaging, Department of Psychology, Sun Yat-Sen University, Guangzhou, 510275, China, and 4Center for Neurobiology and Behavior, Department of Psychiatry, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA

Recent studies have implicated the short allele of the serotonin transporter-linked polymorphic region (5-HTTLPR) in depression vulnerability, particularly in the context of stress. Several neuroimaging studies have shown that 5-HTTLPR genotype predicts amygdala reactivity to negatively valenced stimuli, suggesting a mechanism whereby the short allele confers depression risk. The current study investigated whether 5-HTTLPR genotype similarly affects neural activity during an induced sad mood and during recovery from sad mood. Participants were 15 homozygous short (S) and 15 homozygous long (L) individuals. Regional cerebral blood flow was measured with perfusion functional magnetic resonance imaging during four scanning blocks: baseline, sad mood, mood recovery and following return to baseline. Comparing mood recovery to baseline, both whole brain analyses and template-based region-of-interest analyses revealed greater amygdala activity for the S vs the L-group. There were no significant amygdala differences found during the induced sad mood. These results demonstrate the effect of the S allele on amygdala activity during intentional mood regulation and suggest that amygdala hyperactivity during recovery from a sad mood may be one mechanism by which the S allele confers depression risk.

Keywords: mood; genetics; amygdala; depression; cognitive neuroscience

Correspondence should be addressed to Seth J. Gillihan, Center for the Treatment and Study of Anxiety, Department of Psychiatry, University of Pennsylvania School of Medicine, 3535 Market Street, 6th Floor, Philadelphia, PA 19104, USA. E-mail: gillihan{at}mail.med.upenn.edu

Received March 17, 2009. Accepted July 29, 2009.


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