Our predictions were as follows Method br Results study

Our predictions were as follows: Method
Results study 1 To test whether variation in normative exposure to adverse early-life events was associated with children’s reward-based learning, we correlated Total Adversity scores computed from the ELEQ with reward and loss-related learning from PST testing phase data. Adversity was positively correlated with reward-related learning, r(38)=0.547, p=0.002 (Fig. 1A), but not loss-related learning, r(38)=0.189, p=0.242 (Fig. 1B). To test whether variation in normative exposure to adverse early-life events was associated with children’s reward-based decision-making, we correlated Total Adversity scores computed from the ELEQ with delay discounting parameter estimates. Adversity was positively correlated with discounting parameter magnitude, r(38)=0.35, p=0.027, indicating that LY 2109761 Supplier higher adversity scores were associated with more impulsive choice (Fig. 1C). Age was not related to any learning (reward-related r(38)=0.097, p=0.551; loss-related r(38)=−0.054, p=0.741) or decision-making measures (delay-discounting r(38)=0.143, p=0.377).
Methods study 2
Results study 2
Discussion First, we found that early-life adversity predicts differences in typically developing children’s reward-based learning and decision-making. Adversity experienced early in development has been linked to increased impulsivity and reward incentive salience, both in animals and in humans (Chugani et al., 2001; Hall, 1998; Pollak et al., 2010). In rats, maternal-separation and isolate-rearing increase impulsivity and hyperactivity, with effects more pronounced in measures of impulsive action than impulsive choice (Lovic et al., 2011). In humans, exposure to adversity early in life is associated with heightened ADHD symptomology including greater impulsivity and hyperactivity (Laucht et al., 2007). In the current study, we found that children who had experienced more frequent and intense adverse events early in life discounted temporally displaced rewards more steeply and showed potentiated reward-based learning as compared to children who had experienced less frequent and intense adverse early life events. Interestingly, the association between adversity and learning was specific to aspects of approach learning, including the likelihood of selecting previously rewarded stimuli and RL-model estimates of learning rate to gains. There were no corresponding associations between adversity and avoidance learning. Second, we found that the link between adversity and reward-processing could be explained, at least in part, by differences in ventral striatal response to rewards. Consistent with earlier studies (Pessiglione et al., 2006), rewards were associated with activity in the VS and the vmPFC, and reward-related activity in these regions predicted reward-related learning, including RL-model estimates of learning rate to gains. Interestingly, of these two regions, it was the VS that partially mediated the association between adversity and learning rate to gains. Taken together then, our findings point to a link between adversity, VS physiology, and reward-related behavior. One plausible explanation for our findings is that early adversity contributes to hyper-dopaminergic functioning in the VS. Indeed, pharmacologically induced changes in striatal DA impact VS activity and reward-based learning in ways that are similar to variations in adversity; an increase in striatal DA induced by the anti-Parkinsonian medication L-DOPA for example, increases learning rates and VS response to gains but has no effect on learning and striatal response to losses (Pessiglione et al., 2006). The idea that early adversity contributes to hyper-dopaminergic functioning in the VS is certainly consistent with evidence from animal studies and recent human imaging studies (Egerton et al., 2016; Oswald et al., 2014). In rodents, for example, early adversity has been linked to increases in tonic and phasic DA, as reflected in measures of basal DA (Abercrombie et al., 1989; Hall et al., 1998) and evoked response to amphetamine administration (Piazza and Le Moal 1996) respectively. Similarly in humans, adversity experienced in childhood has been associated with elevated levels of dopamine in adulthood (Egerton et al., 2016), and increased ventral striatal dopamine response to amphetamine. In other cases however, there appears to be a blunted sensitivity to rewards as measured by fMRI (Boecker et al., 2014; Dillon et al., 2009; Hanson et al., 2016; Mehta et al., 2010; Weller and Fisher, 2012), which may be indicative of hypo-dopaminergic striatal functioning; these contradictory findings may be a result of differences in the timing, type, and severity of adversity experienced.