Regulatory variant of the TPH2 gene and early life stress are associated with heightened attention to social signals of fear in infants.

Background: Cross-species evidence suggests that genetic and experiential factors act early in development to establish individual emotional traits, but little is known about the mechanisms that emerge during this period to mediate long-term outcomes. Here, we tested the hypothesis that known genetic and environmental risk conditions may heighten infants' natural tendency to attend to threat-alerting stimuli, resulting in a cognitive bias that may contribute to emotional vulnerability. Methods: Data from two samples of 5-7-month-old infants (N = 139) were used to examine whether established candidate variations in the serotonin-system genes, i.e., TPH2 SNP rs4570625 (-703 G/T) and HTR1A SNP rs6295 (-1019 G/C), and early rearing condition (maternal stress and depressive symptoms) are associated with alterations in infants' attention to facial expressions. Infants were tested with a paradigm that assesses the ability to disengage attention from a centrally presented stimulus (a nonface control stimulus or a neutral, happy, or fearful facial expression) toward the location of a new stimulus in the visual periphery (a geometric shape). Results: TPH2 -703 T-carrier genotype (i.e., TT homozygotes and heterozygotes), presence of maternal stress and depressive symptoms, and a combination of the T-carrier genotype and maternal depressive symptoms were associated with a relatively greater difficulty disengaging attention from fearful facial expressions. No associations were found with infants' temperamental traits. Conclusions: Alterations in infants' natural attentional bias toward fearful facial expressions may emerge prior to the manifestation of emotional and social behaviors and provide a sensitive marker of early emotional development. [ABSTRACT FROM AUTHOR]