Stress-related research has employed several procedures to activate the human stress system. Two of the most commonly used laboratory paradigms are the Trier Social Stress Test (TSST) and the Cold Pressor Test (CPT). We combined their most stressful features to create a simple laboratory stress test capable of eliciting strong autonomic and glucocorticoid stress responses. In comparison with the CPT and its variations, our stress tool (labeled the Maastricht Acute Stress Test; MAST) was found to yield superior salivary cortisol responses, while being equally effective in eliciting subjective stress reactions and (systolic and diastolic) blood pressure increases (study 1; N=80). In study 2 (N=20), we directly compared the effectiveness of the MAST and TSST and found that both methods elicited similar subjective, salivary alpha-amylase, and salivary cortisol stress responses. Finally, we developed and evaluated an appropriate no-stress control version of the MAST that was similar to the stress version, although it did not comprise stressful components (study 3; N=40). Collectively, our results confirm the effectiveness of the MAST in terms of subjective, autonomic, and--most importantly--glucocorticoid stress responses. Thus, as a brief and simple stress protocol, the MAST holds considerable promise for future research.

Stressful events have a major impact on memory. They modulate memory formation in a time-dependent manner, closely linked to the temporal profile of action of major stress mediators, in particular catecholamines and glucocorticoids. Shortly after stressor onset, rapidly acting catecholamines and fast, non-genomic glucocorticoid actions direct cognitive resources to the processing and consolidation of the ongoing threat. In parallel, control of memory is biased towards rather rigid systems, promoting habitual forms of memory allowing efficient processing under stress, at the expense of "cognitive" systems supporting memory flexibility and specificity. In this review, we discuss the implications of this shift in the balance of multiple memory systems for the dynamics of the memory trace. Specifically, stress appears to hinder the incorporation of contextual details into the memory trace, to impede the integration of new information into existing knowledge structures, to impair the flexible generalisation across past experiences, and to hamper the modification of memories in light of new information. Delayed, genomic glucocorticoid actions might reverse the control of memory, thus restoring homeostasis and "cognitive" control of memory again.

Asymmetry in frontal electrical activity has been suggested to index tendencies in affective responding and thus may be associated with hormonal stress responses. To assess the functional role of frontal asymmetry (FA) in stress, we measured FA at rest and following exposure to acute stress induced with the Maastricht Acute Stress Task (MAST; N=70) in the standard 8-13Hz band as well as based on individual alpha frequency (IAF) band. IAF-based resting FAF4-F3 was associated with the stress-induced neuroendocrine response, such that left individual frontal activity predicted smaller total cortisol increases in response to the MAST. Like previous studies, we found resting left-sided FAF8-F7 to predict trait behavioural activation measured with the BIS/BAS scales. FA remained unaffected by stress-induced cortisol response. These findings suggest that individual FA might reflect a trait-like characteristic that moderates the stress response. Our results underscore the utility of IAF in studying individual differences in stress responding.

Stress-induced changes in functional brain connectivity have been linked to the etiology of stress-related disorders. Resting state functional connectivity (rsFC) is especially informative in characterizing the temporal trajectory of glucocorticoids during stress adaptation. Using the imaging Maastricht Acute Stress Test (iMAST), we induced acute stress in 39 healthy volunteers and monitored the neuroendocrine stress levels during three runs of resting state functional magnetic resonance imaging (rs-fMRI): before (run 1), immediately following (run 2), and 30min after acute stress (run 3). The iMAST resulted in strong increases in cortisol levels. Whole-brain analysis revealed that acute stress (run 2 - 1) was characterized by changes in connectivity of the amygdala with the ventrolateral prefrontal cortex (vlPFC), ventral posterior cingulate cortex (PCC), cuneus, parahippocampal gyrus, and culmen. Additionally, cortisol responders were characterized by enhanced amygdala - medial prefrontal cortex (mPFC) connectivity. Stress recovery (run 3 - 2) was characterized by altered amygdala connectivity with the dorsolateral prefrontal cortex (dlPFC), ventral and dorsal anterior cingulate cortex (ACC), anterior hippocampal complex, cuneus, and presupplementary motor area (preSMA). Opposite to non-responders, cortisol responders were characterized by enhanced amygdala connectivity with the anterior hippocampal complex and parahippocampal gyrus, and reduced connectivity with left dlPFC, dACC, and culmen during early recovery. Acute stress responding and recovery are thus associated with changes in the functional connectivity of the amygdala network. Our findings show that these changes may be regulated via stress-induced neuroendocrine levels. Defining stress-induced neuronal network changes is pertinent to developing treatments that target abnormal neuronal activity.

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Instrumental learning, i.e., learning that specific behaviors lead to desired outcomes, occurs through goal-directed and habit memory systems. Exposure to acute stress has been shown to result in less goal-directed control, thus rendering behavior more habitual. The aim of the current studies was to replicate and extend findings on stress-induced prompting of habitual responding and specifically focused on the role of stress-induced cortisol reactivity. Study 1 used an established outcome devaluation paradigm to assess goal-directed and habitual control. Study 2 utilized a modified version of this paradigm that was intended to establish stronger habitual responding through more extensive reward training and applying a relevant behavioral devaluation procedure (i.e., eating to satiety). Both studies failed to replicate that stress overall, i.e., independent of cortisol reactivity, shifted behavior from goal-directed to habitual control. However, both studies found that relative to stress-exposed cortisol non-responders and no-stress controls, participants displaying stress-induced cortisol reactivity displayed prominent habitual responding. These findings highlight the importance of stress-induced cortisol reactivity in facilitating habits.

Frontal alpha asymmetry, a biomarker derived from electroencephalography (EEG) recordings, has often been associated with psychological adjustment, with more left-sided frontal activity predicting approach motivation and lower levels of depression and anxiety. This suggests high relevance to post-traumatic stress disorder (PTSD), a disorder comprising anxiety and dysphoria symptoms. We review this relationship and show that frontal asymmetry can be plausibly linked to neuropsychological abnormalities seen in PTSD. However, surprisingly few studies (k = 8) have directly addressed frontal asymmetry in PTSD, mostly reporting that trait frontal asymmetry has little (if any) predictive value. Meanwhile, preliminary evidence suggest that state-dependent asymmetry during trauma-relevant stimulation distinguishes PTSD patients from resilient individuals. Thus, exploring links between provocation-induced EEG asymmetry and PTSD appears particularly promising. Additionally, we recommend more fine-grained analyses into PTSD symptom clusters in relation to frontal asymmetry. Finally, we highlight hypotheses that may guide future research and help to fully apprehend the practical and theoretical relevance of this biological marker.

Frontal asymmetry in alpha oscillations is assumed to be associated with psychopathology and individual differences in emotional responding. Brain-activity-based feedback is a promising tool for the modulation of cortical activity. Here, we validated a neurofeedback protocol designed to change relative frontal asymmetry based on individual alpha peak frequencies, including real-time average referencing and eye-correction. Participants (N = 60) were randomly assigned to a right, left or placebo neurofeedback group. Results show a difference in trainability between groups, with a linear change in frontal alpha asymmetry over time for the right neurofeedback group during rest. Moreover, the asymmetry changes in the right group were frequency and location specific, even though trainability did not persist at 1 week and 1 month follow-ups. On the behavioral level, subjective stress on the second test day was reduced in the left and placebo neurofeedback groups, but not in the right neurofeedback group. We found individual differences in trainability that were dependent on training group, with participants in the right neurofeedback group being more likely to change their frontal asymmetry in the desired direction. Individual differences in trainability were also reflected in the ability to change frontal asymmetry during the feedback.