Adaptive behavior in a changing world requires flexibly adapting one’s rate of learning to the rate of environmental change. Recent studies have examined the computational mechanisms by which various environmental factors determine the impact of new outcomes on existing beliefs (i.e., the ‘learning rate’). However, the brain mechanisms, and in particular the neuromodulators, involved in this process are still largely unknown. The brain-wide neurophysiological effects of the catecholamines norepinephrine and dopamine on stimulus-evoked cortical responses suggest that the catecholamine systems are well positioned to regulate learning about environmental change, but more direct evidence for a role of this system is scant. Here, we report evidence from a study employing pharmacology, scalp electrophysiology and computational modeling (N = 32) that suggests an important role for catecholamines in learning rate regulation. We found that the P3 component of the EEG—an electrophysiological index of outcome-evoked phasic catecholamine release in the cortex—predicted learning rate, and formally mediated the effect of prediction-error magnitude on learning rate. P3 amplitude also mediated the effects of two computational variables—capturing the unexpectedness of an outcome and the uncertainty of a preexisting belief—on learning rate. Furthermore, a pharmacological manipulation of catecholamine activity affected learning rate following unanticipated task changes, in a way that depended on participants’ baseline learning rate. Our findings provide converging evidence for a causal role of the human catecholamine systems in learning-rate regulation as a function of environmental change.

There is a tremendous global and national (US) burden associated with alcohol misuse and alcohol use disorder (AUD). Further, of the mental health disorders, AUD has the widest treatment gap. Thus, there is a critical need for improved understanding of the etiology, maintenance, and treatment of AUD. The application of cognitive science to the study of AUD has a longstanding history of attempting to meet this need. In this selective review, we identified and focused on four domains of recent (i.e., in the last decade) applications of cognitive science to the study of AUD: implicit cognitive biases, executive function, behavioral economic approaches to alcohol decision making, and functional connectivity neuroimaging. We highlighted advances within these four domains and considered them in the context of dual process models of addiction, which focus on the contribution and interplay of two complementary neurocognitive systems (impulsive and control systems). Findings across the domains were generally consistent with dual process models. They also suggest the need for further model refinements, including integrating behavioral economic approaches and findings from functional connectivity neuroimaging studies. Research evaluating candidate interventions associated with these domains is emergent but promising, suggesting important directions for future research.

Our brains are highly responsive to novelty. However, how novelty is processed in the brain, and what neurotransmitter systems play a role therein, remains elusive. Here, we systematically review studies on human participants that have looked at the neuromodulatory basis of novelty detection and processing. While theoretical models and studies on nonhuman animals have pointed to a role of the dopaminergic, cholinergic, noradrenergic and serotonergic systems, the human literature has focused almost exclusively on the first two. Dopamine was found to affect electrophysiological responses to novelty early in time after stimulus presentation, but evidence on its effects on later processing was found to be contradictory: While neuropharmacological studies mostly yielded null effects, gene studies did point to an important role for dopamine. Acetylcholine seems to dampen novelty signals in the medial temporal lobe, but boost them in frontal cortex. Findings on 5-HT (serotonin) were found to be mostly contradictory. Two large gaps were identified in the literature. First, few studies have looked at neuromodulatory influences on behavioral effects of novelty. Second, no study has looked at the involvement of the noradrenergic system in novelty processing.

Response inhibition is an essential control function necessary to adapt one’s behavior. This key cognitive capacity is assumed to be dependent on the prefrontal cortex and basal ganglia. It is unresolved whether varying inhibitory demands engage different control mechanisms or whether a single motor inhibitory mechanism is involved in any situation. We addressed this question by comparing electrophysiological activity in conditions that require stopping a response to conditions that require switching to an alternate response. Analyses of electrophysiological data obtained from stop-signal tasks are complicated by overlapping stimulus-related activity that is distributed over frontal and parietal cortical recording sites. Here, we applied Laplacian transformation and independent component analysis (ICA) to overcome these difficulties. Participants were faster in switching compared to stopping a response, but we did not observe differences in neural activity between these conditions. Both stop- and change-trials Laplacian transformed ERPs revealed a comparable bilateral parieto-occipital negativity around 180 ms and a frontocentral negativity around 220 ms. ICA results suggested an inhibition-related frontocentral component which was characterized by a negativity around 200 ms with a likely source in anterior cingulate cortex. The data provide support for the importance of posterior mediofrontal areas in inhibitory response control and are consistent with a common neural pathway underlying stopping and changing a motor response. The methodological approach proved useful to distinguish frontal and parietal sources despite similar timing and the ICA approach allowed assessment of single-trial data with respect to behavioral data.