The preponderance of laboratory behavioral evidence suggests
The preponderance of laboratory behavioral evidence suggests that hypersensitivity to rewards may serve as a characteristic or liability factor for DBD (reviewed in Byrd et al., 2014), especially in DBD youth with low levels of anxiety and those exhibiting callous-unemotional (e.g., lack of empathy/guilt) traits (O’Brien et al., 1994). For example, hospitalized adolescents with DBD emit more frequent free-operant responses for reward in a task that rewards each press as a function of time since last press (Dougherty et al., 2003). Moreover, when their lower IQ was controlled for, these patients also showed increased choices of smaller immediate rewards over larger-but delayed rewards in an “experiential” variant of the discrete-choice delay-discounting task (where subjects had to sit and acutely endure the delays). In adulthood, individuals with SUD tend to value smaller immediate rewards over larger delayed rewards on discounting tasks (Kirby et al., 1999), and this response style is particularly pronounced in individuals with SUD and features of CD (Petry, 2002; Bjork et al., 2004a; Bobova et al., 2009). These findings parallel animal literature, in that rodents with a reward-dominant style prior to drug exposure more rapidly self-administer cocaine (Dalley et al., 2007; Belin et al., 2008) and exhibit punishment resistant drug-seeking behavior (Belin et al., 2008; Economidou et al., 2009a,b) relative to control rodents. Although reversal-learning decision tasks do not directly probe reward-sensitivity per se, the deficits in reversal learning performance characteristic of drug abusers or subjects at risk for drug use (Izquierdo and Jentsch, 2012), may exaggerate the effects of reward sensitivity. For example, children and adolescents with externalizing disorders (CD in particular) and those exhibiting callous-unemotional traits continue responding to previously rewarded cues even when contingencies change and the response results in escalating punishments (Fonseca and Yule, 1995; Ernst et al., 2003; Matthys et al., 2004; Byrd et al., 2014), similar to substance abusing adolescents and adults (Damasio et al., 2000; Lane et al., 2007). Decrements in reversal learning are thought to contribute to addiction if the subject is insensitive to increasing negative consequences of substance use An important counterpoint to this narrative, however, is the reward deficiency ANA 12 (RDH) of addiction (Blum et al., 2000). The RDH attributes substance use initiation, and especially chronic use of substances, to a hypofunctioning reward system. Drugs of abuse, by virtue of their ability to trigger a dopamine surge, are uniquely able to stimulate deficient mesolimbic incentive neurocircuitry compared to natural rewards, leading to a bias toward drugs. This bias may be especially critical when substances of abuse themselves degrade mesolimbic function with repeated exposure (Koob and Le Moal, 2008). Evidence for the RDS in fMRI findings is mixed, however, with studies showing both greater as well as lesser mesolimbic responses to reward prospects or deliveries in abusers of alcohol and cannabis (Hommer et al., 2011). Studies of tobacco smokers, however, consistently show reduced VS activation by rewards in accord with the RDH including in teens (Peters et al., 2011). This may be a specific effect of nicotinic acetylcholine desensitization with chronic exposure (or perhaps acute nicotine withdrawal) to reduce phasic stimulus-elicited dopamine responses (Faure et al., 2014). In addition to evidence for greater reward-sensitivity in at-risk youth, problems with cognitive control have also been implicated in the development of both DBD and SUD. Cognitive control refers to a set of abilities necessary to engage in adaptive decision-making in response to changing environmental demands, including sustained attention, response inhibition, and performance monitoring. Children and adolescents with CD exhibit performance deficits on cognitive control tasks compared to normally developing youth (Oosterlaan et al., 1998; Toupin et al., 2000; Loeber et al., 2007), as do adolescents with a history of chronic and problematic substance use (Tapert and Brown, 2000; Medina et al., 2007). In addition, problems with cognitive control appear to be particularly pronounced in individuals with SUD and a history of early CD (Finn et al., 2002). While chronic substance use may cause cognitive control deficits over time (Tapert et al., 2002b), poor performance on cognitive control tasks has been shown to prospectively predict the development of heavy and problematic substance use (Aytaclar et al., 1999; Tapert et al., 2002a). In a longitudinal study, Castellanos-Ryan et al. (2011) administered neurocognition measures to mid-adolescents and found that the link between sensation-seeking personality at 14 and binge drinking at 16 was mediated by reward sensitivity measured in an incentivized go–nogo task, and the link between self-reported impulsivity at 14 and actual CD symptoms at 16 was mediated by inhibitory task performance. To reiterate, whereas an aberrant opponent-process between reward-motivation and inhibition neurocircuity has been postulated to underlie normative developmental differences between adolescents and other age groups in risky behavior, an equally compelling case could be made that an aberrant opponent process is what underlies individual differences between adolescents in neurocircuit function- to promote greater risk of addiction, criminal offending, and violence in some individuals. This is illustrated in Fig. 1.