Altered timing of amygdala activation during sad mood elaboration as a function of 5-HTTLPR

Daniella J. Furman, J. Paul Hamilton, Jutta Joormann, Ian H. Gotlib

Research output: Contribution to journalArticle

29 Scopus citations

Abstract

A functional variant of the serotonin transporter gene (5-HTTLPR) has been associated with increased risk for major depression in the context of stress. In attempting to understand the mechanisms underlying this relation, we tested the hypothesis that 5-HTTLPR genotype affects the speed with which amygdala is recruited during emotional processing in young girls with no history of psychiatric disorder. We used functional magnetic resonance imaging to compare the rise time to peak amygdala activation in 5-HTTLPR short-allele carriers and long-allele homozygotes during enhancement of sad mood. Relative to long-allele homozygotes, participants with at least one copy of the 5-HTTLPR short allele showed both stronger and earlier activation in left amygdala as they increased a sad mood state. Individuals carrying the short allele appear to exhibit a neural 'readiness' to engage and enhance negative affect. Future research should examine how exposure to negative life events and more chronic sadness modify the time course of amygdala activity during the experience of negative emotion.

Original languageEnglish
Article numbernsq029
Pages (from-to)270-276
Number of pages7
JournalSocial Cognitive and Affective Neuroscience
Volume6
Issue number3
DOIs
StatePublished - Jun 1 2011

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Keywords

  • Amygdale
  • Emotion
  • fMRI
  • Genetics

ASJC Scopus subject areas

  • Cognitive Neuroscience
  • Experimental and Cognitive Psychology

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