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Acute stress has been found to impair goal-directed instrumental behaviour, a cognitively flexible behaviour that requires cognitive control. The current study aimed to investigate the role of individual differences in baseline and stress-induced changes in working memory (WM) on the shift to less goal-directed responding under stress. To this end, 112 healthy participants performed an instrumental learning task. In phase 1, participants learned instrumental actions that were associated with two different food rewards. In phase 2, one of these food rewards was devalued by eating until satiety. Before the extinction test in phase 3, participants were subjected to the Maastricht Acute Stress Test or a no-stress control procedure. Results showed that the effect of stress on instrumental behaviour is modulated by baseline, but not stress-induced changes in WM capacity. Specifically, only at low baseline WM capacity did stress induce a shift to less goal-directed behaviour. These findings highlight that our cognitive resources are limited and for those who already have limited resources at baseline taking into account motivational value is impaired under stress., (Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.)

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.

It is generally thought that the effect of acute stress on higher-order functions such as working memory is, for an important part, mediated by central catecholamine activity. However, little is known about the association between neuroendocrine stress responses and catecholamine-dependent working memory-related brain function in the absence of stress. Here, we investigate for the first time in healthy humans (n = 18) how neuroendocrine responses to stress (cortisol and alpha-amylase) relate to fronto-parietal working memory activity changes in response to atomoxetine, a noradrenaline transporter inhibitor that selectively increases extracellular cortical dopamine and noradrenaline. We observed positive correlations between stress-induced cortisol (Pearson's r = 0.75, P < 0.001) and alpha amylase (r = 0.69, P = 0.02) increases and catecholamine-dependent working memory-related activity in dorsolateral prefrontal cortex. Stress-induced cortisol increases furthermore correlated with supramarginal gyrus working memory-related activity (r = 0.79, P < 0.001). Comparing high vs low stress responders revealed that these correlations were driven by decreased working memory activity on placebo and greater working memory activity increases following atomoxetine in high stress responders. These results further corroborate the notion that neuroendocrine responses to stress are an informative proxy of catecholamine function relevant to higher order functions and provide novel hints on the complex relationship between acute stress, catecholamine function and working memory., (© The Author (2017). Published by Oxford University Press.)

Objective: Given the impact of individuals' habits on health, it is important to study how behaviors can become habitual. Cortisol has been well documented to have a role in habit formation. This study aimed to elucidate the influence of the circadian rhythm of cortisol on habit formation in a real-life setting., Method: Forty-eight students were followed for 90 days during which they attempted to adopt a health behavior (psoas iliac stretch). They were randomly assigned to perform the stretch either upon waking in the morning, when cortisol concentrations are high, or before evening bedtime, when cortisol levels approach the nadir. A smartphone application was used to assess the Self-Report Behavioural Automaticity Index every day and to provide reminders for salivary measurements every 30 days. The speed of the health habit formation process was calculated by modeling the learning curves., Results: Extrapolation of the curves indicated that the morning group achieved automaticity at an earlier time point (105.95 days) than did the evening group (154.01 days). In addition, the cortisol level during the performance of the health behavior was identified as a significant mediator of the time point when the health behavior became habitual., Conclusion: The present findings suggest that the time course of the development of healthy habits depends on the time of the day and that the effect is mediated through diurnal variation in cortisol levels. Future studies are now needed to determine to what extent cortisol rhythmicity can help individuals to adopt new health behaviors. (PsycINFO Database Record, ((c) 2017 APA, all rights reserved).)

Reliably eliciting acute stress repeatedly over time is of indispensable value for research into stress vulnerability and for developing interventions aimed at increasing stress resiliency. Here, we evaluated whether the Maastricht Acute Stress Test (MAST), a potent stress protocol that combines physical and psychosocial stress components, can be used to reliably elicit subjective and neuroendocrine stress responses multiple times. Sixty healthy undergraduate participants were exposed to the MAST on three occasions, with intervals of three-weeks and one-month in between sessions. Results showed no significant signs of habituation or sensitization to the MAST in terms of subjective or physiological (salivary alpha-amylase and cortisol) stress reactivity. Fifty-nine percent of the sample displayed a significant physiological stress response (i.e., cortisol) to two MAST exposures and 57% to every MAST exposure. This study demonstrates that the MAST can be used to repeatedly induce significant stress responses., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

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., (© The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.)

Background: The aim of this study was to investigate the effects of sad mood on default mode network (DMN) resting-state connectivity in persons with chronic major depressive disorder (cMDD)., Methods: Participants with a diagnosis of cMDD (n=18) and age, gender and education level matched participants without a diagnosis of depression (n=18) underwent a resting-state fMRI scan, before and after a sad mood induction. The posterior cingulate cortex (PCC) was used as a seed for DMN functional connectivity across the two resting-state measurements., Results: Mood ratings decreased in both groups following the sad mood induction procedure. PCC connectivity with the parahippocampal gyrus, the superior temporal gyrus and the anterior inferior temporal cortex increased in cMDD patients following the sad mood induction, whereas it decreased in non-patient controls. PCC connectivity with the anterior prefrontal cortex and the precuneus decreased in cMDD patients following the sad mood induction, whereas it increased in non-patient controls., Limitations: Limitations of this study include the relatively small sample size and lack of a clinical control group., Conclusions: These findings are in line with neurobiological models of depression suggesting that the observed changes in DMN connectivity following the sad mood induction might reflect a failure to exert cognitive control over negative memory retrieval in patients with cMDD., (Copyright © 2016 Elsevier B.V. All rights reserved.)

Corticosteroid hormones, released during stressful encounters, have profound and far-reaching effects on cognition. They are often thought to accomplish these effects primarily via glucocorticoid receptors (GR), but recent findings from rodent and human studies argue for an additional, critical role of the mineralocorticoid receptor (MR) in cognitive changes in response to stress. We propose that the MR initiates rapid changes in the recruitment of specific neural systems, inducing a shift towards cognitively less-demanding processing and allowing a quick and adequate response to the situation. In combination with slower and longer-lasting actions mediated by GR, this shift leads to optimal coping with the ongoing stressful event., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

People often rely on intuitive judgments at the expense of deliberate reasoning, but what determines the dominance of intuition over deliberation is not well understood. Here, we employed a psychopharmacological approach to unravel the role of two major endocrine stress mediators, cortisol and noradrenaline, in cognitive reasoning. Healthy participants received placebo, cortisol (hydrocortisone) and/or yohimbine, a drug that increases noradrenergic stimulation, before performing the cognitive reflection test (CRT). We found that cortisol impaired performance in the CRT by biasing responses toward intuitive, but incorrect answers. Elevated stimulation of the noradrenergic system, however, had no effect. We interpret our results in the context of the dual systems theory of judgment and decision making. We propose that cortisol causes a shift from deliberate, reflective cognition toward automatic, reflexive information processing., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

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., (Copyright © 2016 the authors 0270-6474/16/361429-09$15.00/0.)

Stress is often associated with a tend-and-befriend response, a putative coping mechanism where people behave generously towards others in order to invest in social relationships to seek comfort and mutual protection. However, this increase in generosity is expected to be directed only towards a delimited number of socially close, but not distant individuals, because it would be maladaptive to befriend everyone alike. In addition, the endocrinological stress response follows a distinct temporal pattern, and it is believed that tend-and-befriend tendencies can be observed mainly under acute stress. By contrast, the aftermath (>1h after) of stress is associated with endocrinological regulatory processes that are proposed to cause increased executive control and reduced emotional reactivity, possibly eliminating the need to tend-and-befriend. In the present experiment, we set out to investigate how these changes immediately and >1h after a stressful experience affect social-distance-dependent generosity levels, a phenomenon called social discounting. We hypothesized that stress has a time-dependent effect on social discounting, with decisions made shortly after (20min), but not 90min after stress showing increased generosity particularly to close others. We found that men tested 20min after stressor onset indeed showed increased generosity towards close but not distant others compared to non-stressed men or men tested 90min after stressor onset. These findings contribute to our understanding on how stress affects prosocial behavior by highlighting the importance of social closeness and the timing of stress relative to the decision as modulating factors in this type of decision making in men., (Copyright © 2015 Elsevier Inc. All rights reserved.)