Literature DB >> 27161551

Emotion moderates the association between HTR2A (rs6313) genotype and antisaccade latency.

Mark Mills1, Olivia Wieda2, Scott F Stoltenberg2, Michael D Dodd2.   

Abstract

The serotonin system is heavily involved in cognitive and emotional control processes. Previous work has typically investigated this system's role in control processes separately for cognitive and emotional domains, yet it has become clear the two are linked. The present study, therefore, examined whether variation in a serotonin receptor gene (HTR2A, rs6313) moderated effects of emotion on inhibitory control. An emotional antisaccade task was used in which participants looked toward (prosaccade) or away (antisaccade) from a target presented to the left or right of a happy, angry, or neutral face. Overall, antisaccade latencies were slower for rs6313 C allele homozygotes than T allele carriers, with no effect of genotype on prosaccade latencies. Thus, C allele homozygotes showed relatively weak inhibitory control but intact reflexive control. Importantly, the emotional stimulus was either present during target presentation (overlap trials) or absent (gap trials). The gap effect (slowed latency in overlap versus gap trials) in antisaccade trials was larger with angry versus neutral faces in C allele homozygotes. This impairing effect of negative valence on inhibitory control was larger in C allele homozygotes than T allele carriers, suggesting that angry faces disrupted/competed with the control processes needed to generate an antisaccade to a greater degree in these individuals. The genotype difference in the negative valence effect on antisaccade latency was attenuated when trial N-1 was an antisaccade, indicating top-down regulation of emotional influence. This effect was reduced in C/C versus T/_ individuals, suggesting a weaker capacity to downregulate emotional processing of task-irrelevant stimuli.

Entities:  

Keywords:  Antisaccade; Emotion; Inhibitory control; Serotonin

Mesh:

Substances:

Year:  2016        PMID: 27161551     DOI: 10.1007/s00221-016-4669-6

Source DB:  PubMed          Journal:  Exp Brain Res        ISSN: 0014-4819            Impact factor:   1.972


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