Abstract

The serotonin transporter gene (5-HTTLPR) influences emotional reactivity and attentional bias toward or away from emotional stimuli, and has been implicated in psychopathological states, such as depression and anxiety disorder. The short allele is associated with increased reactivity and attention toward negatively-valenced emotional information, whereas the long allele is associated with increased reactivity and attention toward positively-valenced emotional information. The neural basis for individual differences in the ability to exert cognitive control over these bottom-up biases in emotional reactivity and attention is unknown, an issue investigated in the present study. Healthy adult participants were divided into two groups, either homozygous carriers of the 5-HTTLPR long allele or homozygous carriers of the short allele, and underwent functional magnetic resonance imaging (fMRI) while completing an Emotional Stroop-like task that varied in the congruency of task-relevant and task-irrelevant information and the emotional valence of the task-irrelevant information. Behaviorally, participants demonstrated the classic “Stroop effect” (responses were slower for incongruent than congruent trials), which did not differ by 5-HTTLPR genotype. However, fMRI results revealed that genotype influenced the degree to which neural systems were engaged depending on the valence of the conflicting task-irrelevant information. While the “Long” group recruited prefrontal control regions and superior temporal sulcus during conflict when the task-irrelevant information was positively-valenced, the “Short” group recruited these regions during conflict when the task-irrelevant information was negatively-valenced. Thus, participants successfully engaged cognitive control to overcome conflict in an emotional context using similar neural circuitry, but the engagement of this circuitry depended on emotional valence and 5-HTTLPR status. These results suggest that the interplay between emotion and cognition is modulated, in part, by a genetic polymorphism that influences serotonin neurotransmission.

Highlights

  • How does emotion influence cognition? Here we examine the degree to which cognitive control, the ability to engage in goaldirected behavior, is influenced by salient but task-irrelevant information that is emotional in nature

  • Mean accuracy (% correct) and mean reaction time for correct responses was computed for congruent and incongruent trials for each emotional valence (Table 1) and this was subsequently entered into 2 mixed 2 × 2 × 3 analysis of variance (ANOVA), with genotype (Short, Table 1 | Demographics, cognitive control, and trait affect measures for short and long 5-HTTLPR genotype groups; mean (SD)

  • We compared activation for stimuli in which the face had a negative emotion compared to a positive one, which yielded great activation in visual cortex and portions of the superior temporal sulcus for negative compared to positive emotional expressions

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Summary

Introduction

How does emotion influence cognition? Here we examine the degree to which cognitive control, the ability to engage in goaldirected behavior, is influenced by salient but task-irrelevant information that is emotional in nature. The evidence is divided, with some studies suggesting that emotional information can facilitate, impede, or have no effect on cognitive control (Cohen and Henik, 2012). Research has identified factors that can influence or mediate these effects, including the valence of the emotional material (i.e., positive vs negative e.g., Kahan and Hely, 2008), individual differences in negative affect such as anxiety (Cisler and Wolitzky-Taylor, 2011), and genetic polymorphisms that may contribute to these individual differences, such as the serotonin transporter gene (Beevers and Wells, 2009). One of the most replicated findings regarding genetic polymorphisms is that the 5-HTTLPR genotype influences emotional reactivity to negative information (Pergamin-Hight et al, 2012) and sensitivity to stressors (Karg et al, 2011). The L allele contains an A to G single

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