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  • br Brain signatures of increased reward sensitivity and

    2018-11-14


    Brain signatures of increased reward sensitivity and reduced cognitive control in youth with behavior problems As mentioned previously, developmental differences in VS recruitment by rewards during fMRI have been interpreted as reflecting underlying development of DA activity in the mesolimbic system (Luciana et al., 2012). Might individual differences in DA functioning also apply to individual differences in risk traits? In Positron Emission Tomography (PET) studies of adults, displacement of radiolabeled DA ligands in VS by rewards have correlated within-subject with fMRI-measured VS recruitment by rewards (Schott et al., 2008; Buckholtz et al., 2010), and dynamic DA synthesis in VS correlated with sensation-seeking personality (Lawrence and Brooks, 2014). Third, antisocial and psychopathic personality features in adults have been associated with increased amphetamine-induced dopamine release in nucleus accumbens (Buckholtz et al., 2010). Therefore, it stands to reason that individual differences between adolescents in VS responsiveness to fMRI rewards could also be DA-mediated. By extension, greater VS activation by rewards in fMRI might be expected in youth with greater impulsivity or sensation-seeking personality. For example, in adolescents with no psychiatric disorder, individual differences in sensation-seeking (Bjork et al., 2008), and individual differences in a tally of self-reported risky behaviors and substance use (Bjork et al., 2011) correlated positively with mesolimbic recruitment by cues for operant rewards. Moreover, striatal sensitivity to rewards correlated positively with self-reported likelihood to engage in future risky behavior in both adolescents and adults (Galvan et al., 2007). Researchers have also begun directly examining buy ANA 12 function abnormalities in youth with significant antisocial behavior (AB) using cognitive control tasks as well as various monetary reward tasks (recently reviewed in Hyde et al., 2013). These studies collectively implicate (correlate) altered brain activity in limbic circuits (such as insula and VS) in syndromes of antisocial behavior, with differences between findings likely resulting from differing definitions of antisocial behavior such as the presence versus absence psychopathic features, including callous-unemotional traits. For example, adolescents with DBD also showed significantly greater VS recruitment by reward notifications in the MID task (Bjork et al., 2010a). Gatzke-Kopp et al. (2009) reported that when an operant response was no longer rewarded, AB subjects persisted in striatal activation by reward-linked cues, while controls instead recruited error-monitoring circuitry of the ACC when response contingencies changed. In large-scale twin studies of psychiatric diagnoses, a latent neurobiological trait has been suggested that underlies both addiction and DBD (Kendler et al., 2003). Recent functional neuroimaging studies suggest that abnormalities in the neural network subserving cognitive control may represent a mechanism for this latent trait or common risk factor for the development of both CD and SUD. In comparison to controls, adolescents with CD have been shown to exhibit reduced dorsomedial prefrontal activity during attention allocation (Rubia et al., 2009) and reduced posterior ACC and inferior parietal reactivity when committing response inhibition errors (Rubia et al., 2008). Reduced dorsal pre-frontal activation during response inhibition has also been found in adolescents with high levels of neurobehavioral disinhibition, which includes features of CD (McNamee et al., 2008). Individuals with SUD exhibit similar abnormalities, including reduced brain activation in the dorsolateral/dorsomedial prefrontal cortex (Tapert et al., 2001; Eldreth et al., 2004; Chang et al., 2006; Schweinsburg et al., 2008), ACC (Kaufman et al., 2003; Bolla et al., 2004; Eldreth et al., 2004; Forman et al., 2004; Lee et al., 2005; Li et al., 2008), and posterior parietal cortex (Tapert et al., 2001) during cognitive control tasks. However, it remains unclear whether these deficits are a consequence of chronic use, a risk factor for the development SUD, or a combination of the two.