Recent behavioral modeling and pupillometry studies suggest that neuromodulatory arousal systems play a role in regulating decision formation but neurophysiological support for these observations is lacking. We employed a randomized, double-blinded, placebo-controlled, crossover design to probe the impact of pharmacological enhancement of catecholamine levels on perceptual decision-making. Catecholamine levels were manipulated using the clinically relevant drugs methylphenidate and atomoxetine, and their effects were compared with those of citalopram and placebo. Participants performed a classic EEG oddball paradigm that elicits the P3b, a centro-parietal potential that has been shown to trace evidence accumulation, under each of the four drug conditions. We found that methylphenidate and atomoxetine administration shortened RTs to the oddball targets. The neural basis of this behavioral effect was an earlier P3b peak latency, driven specifically by an increase in its buildup rate without any change in its time of onset or peak amplitude. This study provides neurophysiological evidence for the catecholaminergic enhancement of a discrete aspect of human decision-making, that is, evidence accumulation. Our results also support theoretical accounts suggesting that catecholamines may enhance cognition via increases in neural gain.

Disentangling the component processes that contribute to human executive control is a key challenge for cognitive neuroscience. Here, we employ event-related potentials to provide electrophysiological evidence that action errors during a go/no-go task can result either from sustained attention failures or from failures of response inhibition, and that these two processes are temporally and physiologically dissociable, although the behavioral error—a nonintended response—is the same. Thirteen right-handed participants performed a version of a go/no-go task in which stimuli were presented in a fixed and predictable order, thus encouraging attentional drift, and a second version in which an identical set of stimuli was presented in a random order, thus placing greater emphasis on response inhibition. Electrocortical markers associated with goal maintenance (late positivity, alpha synchronization) distinguished correct and incorrect performance in the fixed condition, whereas errors in the random condition were linked to a diminished N2–P3 inhibitory complex. In addition, the amplitude of the error-related negativity did not differ between correct and incorrect responses in the fixed condition, consistent with the view that errors in this condition do not arise from a failure to resolve response competition. Our data provide an electrophysiological dissociation of sustained attention and response inhibition.