Dopaminergic medication increases motivation to exert cognitive control by reducing subjective effort costs in Parkinson's patients.

Engaging in demanding mental activities requires the allocation of cognitive control, which can be effortful and aversive. Individuals thus tend to avoid exerting cognitive effort if less demanding behavioral options are available. Recent accounts propose a key role for dopamine in motivating behavior by increasing the sensitivity to rewards associated with effort exertion. Whether dopamine additionally plays a specific role in modulating the sensitivity to the costs of cognitive effort, even in the absence of any incentives, is much less clear. To address this question, we assessed cognitive effort avoidance in patients (n = 38) with Parkinson's disease, a condition characterized by loss of midbrain dopaminergic neurons, both ON and OFF dopaminergic medication and compared them to healthy controls (n = 24). Effort avoidance was assessed using the Demand Selection Task (DST), in which participants could freely choose between performing a high-demand or a low-demand version of a task-switching paradigm. Critically, participants were not offered any incentives to choose the more effortful option, nor for good performance. While healthy controls and patients OFF their dopaminergic medications consistently preferred the low-demand option, effort avoidance in patients ON dopaminergic medications was reduced compared to patients OFF, a difference which seems to lessen over trials. These differences in preference could not be explained by altered task-switching performance. Although patients ON were less accurate at detecting the different effort levels, as measured during instructed forced-choice blocks, their detection ability was not associated with effort avoidance, unlike in the healthy controls and the patients OFF. Our findings provide evidence that dopamine replacement in Parkinson's patients increases the willingness to engage in cognitively demanding behavior, and that this cannot be explained by possible effects of dopamine replacement on performance nor on the ability to detect effort demands. These results suggest that dopamine plays a role in reducing the sensitivity to effort costs that is independent of its role in enhancing the sensitivity to the benefits of effort exertion.

Cognitive effort exertion enhances electrophysiological responses to rewarding outcomes.

Recent work has highlighted neural mechanisms underlying cognitive effort-related discounting of anticipated rewards. However, findings on whether effort exertion alters the subjective value of obtained rewards are inconsistent. Here, we provide a more nuanced account of how cognitive effort affects subsequent reward processing in a novel task designed to assess effort-induced modulations of the Reward Positivity, an event-related potential indexing reward-related neural activity. We found that neural responses to both gains and losses were significantly elevated in trials requiring more versus less cognitive effort. Moreover, time-frequency analysis revealed that these effects were mirrored in gain-related delta, but not in loss-related theta band activity, suggesting that people ascribed more value to high-effort outcomes. In addition, we also explored whether individual differences in behavioral effort discounting rates and reward sensitivity in the absence of effort may affect the relationship between effort exertion and subsequent reward processing. Together, our findings provide evidence that cognitive effort exertion can increase the subjective value of subsequent outcomes and that this effect may primarily rely on modulations of delta band activity.

Acute Psychosocial Stress Increases Cognitive-Effort Avoidance.

Adverse effects following acute stress are traditionally thought to reflect functional impairments of central executive-dependent cognitive-control processes. However, recent evidence demonstrates that cognitive-control application is perceived as effortful and aversive, indicating that stress-related decrements in cognitive performance could denote decreased motivation to expend effort instead. To investigate this hypothesis, we tested 40 young, healthy individuals (20 female, 20 male) under both stress and control conditions in a 2-day study that had a within-subjects design. Cognitive-effort avoidance was assessed using the demand-selection task, in which participants chose between performing low-demand and high-demand variants of a task-switching paradigm. We found that acute stress indeed increased participants' preference for less demanding behavior, whereas task-switching performance remained intact. Additional Bayesian and multiverse analyses confirmed the robustness of this effect. Our findings provide novel insights into how stressful experiences shape behavior by modulating our motivation to employ cognitive control.

Causal role of the inferolateral prefrontal cortex in balancing goal-directed and habitual control of behavior.

Successful adaptation to complex environments depends on the balance of at least two systems: a flexible but slow goal-directed system encoding action-outcome associations and an efficient but rigid habitual system linking responses to preceding stimuli. Recent evidence suggests that the inferolateral prefrontal cortex (ilPFC), a region well known to contribute to cognitive control processes, may play a crucial role in the balance of goal-directed and habitual responding. This evidence, however, comes mainly from correlational data and whether the ilPFC is indeed causally involved in the goal-directed vs. habitual control of behavior is unclear. Here, we used neuro-navigated theta-burst stimulation (TBS) to either inhibit or enhance right ilPFC functionality before participants completed an instrumental learning task designed to probe goal-directed vs. habitual behavioral control. TBS did not affect overall learning performance. However, participants that had received inhibitory TBS were less able to adapt their behavior to altered task demands, indicating a shift from goal-directed towards more habitual control of behavior. Sham or excitatory TMS groups showed no such effect and were comparable in their performance to an unstimulated control group. Our findings indicate a causal role of the ilPFC in the balance of goal-directed vs. habitual control of behavior.

Transcranial Stimulation Over the Dorsolateral Prefrontal Cortex Increases the Impact of Past Expenses on Decision-Making.

Goal-directed choices should be guided by the expected value of the available options. However, people are often influenced by past costs in their decisions, thus succumbing to a bias known as the "sunk-cost effect." Recent functional magnetic resonance imaging data show that the sunk-cost effect is associated with increased activity in dorsolateral prefrontal cortex (dlPFC) and altered crosstalk of the dlPFC with other prefrontal areas. Are these correlated neural processes causally involved in the sunk-cost effect? Here, we employed transcranial direct current stimulation (tDCS) to examine the role of the dlPFC for biasing choices in line with the cost of past expenses. Specifically, we applied different types of tDCS over the right dlPFC while participants performed an investment task designed to assess the impact of past investments on current choices. Our results show a pronounced sunk-cost effect that was significantly increased by anodal tDCS, but left unaltered by cathodal or sham stimulation. Importantly, choices were not affected by stimulation when no prior investments had been made, underlining the specificity of the obtained effect. Our findings suggest a critical role of the dlPFC in the sunk-cost effect and thus elucidate neural mechanisms by which past investments may influence current decision-making.

Transcranial Stimulation of the Dorsolateral Prefrontal Cortex Prevents Stress-Induced Working Memory Deficits.

Stress is known to impair working memory performance. This disruptive effect of stress on working memory has been linked to a decrease in the activity of the dorsolateral prefrontal cortex (dlPFC). In the present experiment, we tested whether transcranial direct current stimulation (tDCS) of the dlPFC can prevent stress-induced working memory impairments. We tested 120 healthy participants in a 2 d, sham-controlled, double-blind between-subjects design. Participants completed a test of their individual baseline working memory capacity on day 1. On day 2, participants were exposed to either a stressor or a control manipulation before they performed a visuospatial and a verbal working memory task. While participants completed the tasks, anodal, cathodal, or sham tDCS was applied over the right dlPFC. Stress impaired working memory performance in both tasks, albeit to a lesser extent in the verbal compared with the visuospatial working memory task. This stress-induced working memory impairment was prevented by anodal, but not sham or cathodal, stimulation of the dlPFC. Compared with sham or cathodal stimulation, anodal tDCS led to significantly better working memory performance in both tasks after stress. Our findings indicate a causal role of the dlPFC in working memory impairments after acute stress and point to anodal tDCS as a promising tool to reduce cognitive deficits related to working memory in stress-related mental disorders, such as depression, schizophrenia, or post-traumatic stress disorder. SIGNIFICANCE STATEMENT: Working memory deficits are prominent in stress-related mental disorders, such as depression, schizophrenia, or post-traumatic stress disorder. Similar working memory impairments have been observed in healthy individuals exposed to acute stress. So far, attempts to prevent such stress-induced working memory deficits focused mainly on pharmacological interventions. Here, we tested the idea that transcranial direct current stimulation of the dorsolateral prefrontal cortex (dlPFC), a critical neural substrate of working memory, may prevent working memory impairments after stress. Our results indicate that anodal stimulation of the dlPFC may indeed preserve working memory performance under stress, suggesting that the dlPFC plays a causal role in stress-induced working memory deficits and pointing to a potential new avenue to prevent stress-induced cognitive impairments.