Previous work shows that the adolescent reward system is hyperactive, but this finding may be confounded by differences in how teens value money. To address this, we examined the neural ontogeny of objective value representation. Adolescent and adult participants performed a monetary gambling task in which they chose to accept or reject gambles of varying expected value. Increasing expected value had a stronger influence over gambling choices in adolescents relative to adults, an effect that was paralleled by greater activation in the ventral striatum in adolescents. This unique adolescent ventral striatum response remained even after matching groups on acceptance behavior. These behavioral and neural data suggest that the value of available options has a greater influence in adolescent versus adult choices, even when objective value and subjective choice are held constant. This research provides further evidence that hyperactivation of reward circuitry in adolescence may be a normative ontogenetic shift that is due to greater valuation in the adolescent brain.A dolescence is characterized by heightened sensitivity to rewards (1). This phenotype is subserved by exaggerated neural response in ventral striatum (VS) to the anticipation (2) and receipt of expected (3-5) and unexpected reward (6) in adolescents versus other age groups. The question remains, however, whether this effect is mediated by ontogenetic differences or simply a methodological consequence of using money as the rewarding stimulus. In other words, does the adolescent brain attribute greater value to available rewards, or is the effect driven by adolescents valuing money to a greater extent than adults because they typically have less access to and experience with it? The goal of this study was to disentangle these possibilities by examining subjective valuation (indexed by behavior) of objectively valued choices.Subjective value (SV) is defined as the value that an individual places on a stimulus (7). To make a choice, an organism determines the SV of each alternative and then selects the one with the greatest SV (8, 9). A recent metaanalysis of 206 studies of SV in adults identified the ventromedial prefrontal cortex (VMPFC) and VS as a "valuation system" (8). These regions represent SV during choice for monetary stimuli (10-14), charitable donations (15), consumer goods (16), and food (17)(18)(19). Despite the wealth of knowledge on the neural correlates of SV in adults, no previous studies have examined the neurobiological development of SV, which precludes ruling out the possibility that previous findings in support of a hyperactive adolescent reward system were confounded by differences in participant valuation.One approach to understanding the neural computation of SV is through measurement of expected value (EV), the sum of all of the possible outcomes of a particular choice multiplied by their probabilities (20). In adults, increasing EV yields parametric activation increases in bilateral VS, midbrain, medial prefrontal cortex (MPFC), an...
Individuals are frequently faced with risky decisions involving the potential for both gain and loss. Exploring the role of both potential gains and potential losses in predicting risk taking is critical to understanding how adolescents and adults make the choice to engage in or avoid a real-life risk. This study aimed to examine the impact of potential losses as well as gains on adolescent decisions during risky choice in a laboratory task. Adolescent (n=18) and adult (n=16) participants underwent functional magnetic resonance imaging (fMRI) during a mixed gambles task, and completed questionnaires measuring real-world risk-taking behaviors. While potential loss had a significantly greater effect on choice than potential gain in both adolescents and adults and there were no behavioral group differences on the task, adolescents recruited significantly more frontostriatal circuitry than adults when choosing to reject a gamble. During risk-seeking behavior, adolescent activation in medial prefrontal cortex (mPFC) was negatively correlated with self-reported likelihood of risk taking. During risk-avoidant behavior, mPFC activation of in adults was negatively correlated with self-reported benefits of risk-taking. Taken together, these findings reflect different neural patterns during risk-taking and risk-avoidant behaviors in adolescents and adults.
Background Higher levels of impulsivity have been implicated in the development of alcohol use disorders. Recent findings suggest that impulsivity is not a unitary construct, highlighted by the diverse ways in which the various measures of impulsivity relate to alcohol use outcomes. This study simultaneously tested the following dimensions of impulsivity as determinants of alcohol use and alcohol problems: risky decision-making, self-reported risk attitudes, response inhibition, and impulsive decision-making. Method Participants were a community sample of non-treatment seeking problem drinkers (N = 158). Structural Equation Modeling (SEM) analyses employed behavioral measures of impulsive decision-making (Delay Discounting Task, DDT), response inhibition (Stop Signal Task, SST), and risky decision-making (Balloon Analogue Risk Task, BART), and a self-report measure of risk attitudes (Domain-specific Risk-attitude Scale, DOSPERT), as predictors of alcohol use and of alcohol-related problems in this sample. Results The model fit well, accounting for 38% of the variance in alcohol problems, and identified two impulsivity dimensions that significantly loaded onto alcohol outcomes: (1) impulsive decision-making, indexed by the DDT; and (2) risky decision-making, measured by the BART. Conclusions The impulsive decision-making dimension of impulsivity, indexed by the DDT, was the strongest predictor of alcohol use and alcohol pathology in this sample of problem drinkers. Unexpectedly, a negative relationship was found between risky decision-making and alcohol problems. The results highlight the importance of considering the distinct facets of impulsivity in order to elucidate their individual and combined effects on alcohol use initiation, escalation, and dependence.
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