The present study centered on the allelic

The present study centered on the allelic variations of the serotonin transporter linked polymorphic region (5-HTTLPR) of the serotonin transporter gene, SLC6A4. Serotonin is the most widely distributed neurotransmitter in the brain, with the serotonin system originating from the raphe nuclei and projecting to a broad range of buy dhpg regions (for a review, see Lesch and Waider, 2012). One of these regions is prefrontal cortex (PFC), which receives direct projections of serotonergic neurons from raphe nuclei and hosts a dense distribution of serotonin receptor and transporter sites (Andrade, 2011; Puig and Gulledge, 2011). PFC is a fundamental component of neural mechanisms involved in selective attention (Degerman et al., 2006; Fritz et al., 2007; Pugh et al., 1996; Wu et al., 2007). PFC is generally considered a source of top-down attentional modulation, which can then influence sensory processing in site-specific regions (Petersen and Posner, 2012; Squire et al., 2013). Given the contributions of serotonin to the development, neuroplasticity and functioning of the frontal cortex in the mammalian brain (Andrade, 2011; Lesch and Waider, 2012; Puig and Gulledge, 2011) and the critical role of prefrontal cortex in selective attention (Bidet-Caulet et al., 2014; Knight et al., 1981), it is plausible that the serotonergic systems play a role in the development of selective attention. A key controller of serotonin functioning in the brain is serotonin transporter (Murphy and Lesch, 2008). 5-HTTLPR is a polymorphic region in the gene that encodes serotonin transporter and is involved in serotonin reuptake from the synaptic cleft to presynaptic nerve terminals (Iurescia et al., 2015; Lesch et al., 1996). There are two predominant allelic variations of 5-HTTLPR: the short allele and the long allele (Heils et al., 1996). The short allele of 5-HTTLPR is generally associated with lower transcriptional activity of the serotonin transporter gene, but the precise neurobiological mechanisms through which these allelic variations contribute to brain functioning have yet to be determined (Iurescia et al., 2015). Despite this uncertainty in specific neurobiological mechanisms, 5-HTTLPR has been the most investigated genetic polymorphism in psychology (Caspi et al., 2010). Most previous research investigated the allelic variations of 5-HTTLPR in the context of susceptibility or resilience to psychopathology (Belsky and Pluess, 2009; Caspi et al., 2010; Karg et al., 2011; Pluess and Belsky, 2013). Accordingly, previous studies on 5-HTTLPR and attention focused predominantly on how this polymorphism relates to biased attention toward stimuli with positive or negative emotional valence, as a potential marker for susceptibility to psychopathology (Pergamin-Hight et al., 2012). Such studies commonly reported that the short allele, either in homozygous and/or heterozygous form, was associated with attentional bias toward emotionally valenced stimuli (Beevers et al., 2009; Fox et al., 2011; Lonsdorf et al., 2014; Osinsky et al., 2008; Thomason et al., 2010). However, little is known about the relationship between 5-HTTLPR and selective attention in young children, or in the absence of emotionally valenced stimuli. In the present study, we assessed the relationship between 5-HTTLPR and the neural mechanisms of selective attention in a sample of 121 preschool-age children from lower socioeconomic status (SES) backgrounds. Event-related brain potentials (ERPs) were used to examine the neural mechanisms of selective auditory attention using a well-established, child-friendly dichotic listening task without emotional valence (Coch et al., 2005; Neville et al., 2013; Sanders et al., 2006; Stevens et al., 2009). We focused on children from lower SES backgrounds, whose selective attention abilities are at heightened risk for deficits (D\'Angiulli et al., 2008; Stevens et al., 2009, 2014), with notable individual differences in vulnerability (Isbell et al., 2016). Based on the structural and functional connections between serotonergic systems and PFC (Andrade, 2011; Lesch and Waider, 2012; Puig and Gulledge, 2011) and the role of PFC as a source of attentional modulation (Bidet-Caulet et al., 2014; Knight et al., 1981), we expected 5-HTTLPR to account for individual differences in the neural mechanisms of selective attention.