The relation between brain development across adolescence and adolescent risky behavior has attracted increasing interest in recent years. It has been proposed that adolescents are hypersensitive to reward because of an imbalance in the developmental pattern followed by the striatum and prefrontal cortex. To date, it is unclear if adolescents engage in risky behavior because they overestimate potential rewards or respond more to received rewards and whether these effects occur in the absence of decisions. In this study, we used a functional magnetic resonance imaging paradigm that allowed us to dissociate effects of the anticipation, receipt, and omission of reward in 10- to 12-year-old, 14- to 15-year-old, and 18- to 23-year-old participants. We show that in anticipation of uncertain outcomes, the anterior insula is more active in adolescents compared with young adults and that the ventral striatum shows a reward-related peak in middle adolescence, whereas young adults show orbitofrontal cortex activation to omitted reward. These regions show distinct developmental trajectories. This study supports the hypothesis that adolescents are hypersensitive to reward and adds to the current literature in demonstrating that neural activation differs in adolescents even for small rewards in the absence of choice. These findings may have important implications for understanding adolescent risk-taking behavior.

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Background: Rivastigmine enhances cholinergic activity and has been shown in clinical trials to decrease the rate of deterioration in Alzheimer's disease. It remains unclear where in the brain it exerts its effect. Functional magnetic resonance imaging (fMRI) can be used to measure changes in brain function and relate these to cognition. Objectives: To use fMRI to study brain activation with rivastigmine treatment. Methods: The effect on brain activation of a single dose of rivastigmine was tested in seven patients with mild Alzheimer's disease using fMRI during face encoding, and in five patients during a parametric working memory task. Results: During face encoding, rivastigmine increased bilateral activation in the fusiform gyrus. Brain activation was also enhanced in the prefrontal cortex in a simple working memory task. When working memory load was further increased, not only was increased activation seen, but in certain areas there was also decreased activation. Conclusions: These findings link the previously observed increase in cognitive performance in Alzheimer's disease after treatment with a cholinesterase inhibitor to altered brain activation. Although the results cannot be generalised to the Alzheimer's disease population at large, they provide evidence that in mild Alzheimer's disease, rivastigmine enhances brain activation in the fusiform and frontal cortices. This is compatible with the concept of cholinergic circuitry.

RationaleAlthough risky decision-making is one of the hallmarks of alcohol use disorders, relatively little is known about the acute psychopharmacological effects of alcohol on decision-making processes.ObjectiveThe present study investigated the acute effects of alcohol on neural mechanisms underlying feedback processing and outcome evaluation during risky decision-making, using event-related brain potentials (ERPs).MethodsERPs elicited by positive and negative feedback were recorded during performance of a modified version of the Balloon Analogue Risk Task in male participants receiving either a moderate dose of alcohol (0.65 g/kg alcohol; n = 32) or a non-alcoholic placebo beverage (n = 32).ResultsOverall, there was no significant difference in the mean number of pumps between the alcohol and the placebo condition. However, when analyzing over time, it was found that the alcohol group made more riskier choices at the beginning of the task than the placebo group. ERPs demonstrated that alcohol consumption did not affect early processing of negative feedback, indexed by the feedback-related negativity. By contrast, alcohol-intoxicated individuals showed significantly reduced P300 amplitudes in response to negative feedback as compared to sober controls, suggesting that more elaborate evaluation to losses was significantly diminished.ConclusionsThese results suggest that alcohol consumption does not influence the ability to rapidly evaluate feedback valence, but rather the ability to assign sufficient attention to further process motivationally salient outcomes. Blunted P300 amplitudes may reflect poor integration of feedback across trials, particularly adverse ones. Consequently, alcohol may keep people from effectively predicting the probability of future gains and losses based on their reinforcement history.