Acute stress differentially affects spatial configuration learning in high and low cortisol-responding healthy adults

Background: Stress and stress hormones modulate memory formation in various ways that are relevant to our understanding of stress-related psychopathology, such as posttraumatic stress disorder (PTSD). Particular relevance is attributed to efficient memory formation sustained by the hippocampus and parahippocampus. This process is thought to reduce the occurrence of intrusions and flashbacks following trauma, but may be negatively affected by acute stress. Moreover, recent evidence suggests that the efficiency of visuo-spatial processing and learning based on the hippocampal area is related to PTSD symptoms. Objective: The current study investigated the effect of acute stress on spatial configuration learning using a spatial contextual cueing task (SCCT) known to heavily rely on structures in the parahippocampus. Method: Acute stress was induced by subjecting participants (N = 34) to the Maastricht Acute Stress Test (MAST). Following a counterbalanced within-subject approach, the effects of stress and the ensuing hormonal (i.e., cortisol) activity on subsequent SCCT performance were compared to SCCT performance following a no-stress control condition. Results: Acute stress did not impact SCCT learning overall, but opposing effects emerged for high versus low cortisol responders to the MAST. Learning scores following stress were reduced in low cortisol responders, while high cortisol-responding participants showed improved learning. Conclusions: The effects of stress on spatial configuration learning were moderated by the magnitude of endogenous cortisol secretion. These findings suggest a possible mechanism by which cortisol responses serve an adaptive function during stress and trauma, and this may prove to be a promising route for future research in this area

Facing stress: no effect of acute stress at encoding or retrieval on face recognition memory

Eyewitnesses may experience stress during a crime and when attempting to identify the perpetrator subsequently. Laboratory studies can provide insight into how acute stress at encoding and retrieval affects memory performance. However, previous findings exploring this issue have been mixed. Across two preregistered experiments, we examined the effects of stress during encoding and retrieval on face and word recognition performance. We used the Maastricht Acute Stress Test (MAST) to induce stress and verified the success of the stress manipulation with blood pressure measures, salivary cortisol levels, and negative affect scores. To examine differences in stressor timing, participants encoded target faces or words both when confronted with the stressor and during the subsequent cortisol peak and retrieved these stimuli 24 h later. We found neither effects of acute stress on face recognition memory during encoding or retrieval (Experiments 1 and 2), nor effects of encoding stress on word recognition memory (Experiment 2). Bayesian analyses largely provided substantial or strong evidence for the null hypotheses. We emphasize the need for well-powered experiments using contemporary methodology for a more complete understanding of the effect of acute stress on face recognition memory

The effects of stress on eyewitness memory: a survey of memory experts and laypeople

This survey examined lay and expert beliefs about statements concerning stress effects on (eyewitness) memory. Thirty-seven eyewitness memory experts, 36 fundamental memory experts, and 109 laypeople endorsed, opposed, or selected don’t know responses for a range of statements relating to the effects of stress at encoding and retrieval. We examined proportions in each group and differences between groups (eyewitness memory experts vs. fundamental memory experts; experts vs. laypeople) for endorsements (agree vs. disagree) and selections (don’t know vs. agree/disagree). High proportions of experts from both research fields agreed that very high levels of stress impair the accuracy of eyewitness testimony. A majority of fundamental experts, but not eyewitness experts, endorsed the idea that stress experienced during encoding can enhance memory. Responses to statements regarding moderating factors such as stressor severity and detail type provided further insight into this discrepancy. Eyewitness memory experts more frequently selected the don’t know option for neuroscientific statements regarding stress effects on memory than fundamental memory experts, although don’t know selections were substantial among both expert groups. Laypeople’s responses to eight of the statements differed statistically from expert answers on topics such as memory in children, in professionals such as police officers, for faces and short crimes, and the existence of repression, providing insight into possible ‘commonsense’ beliefs on stress effects on memory. Our findings capture the current state of knowledge about stress effects on memory as reflected by sample of experts and laypeople, and highlight areas where further research and consensus would be valuabl

The interaction between stress and chronic pain through the lens of threat learning

Stress and pain are interleaved at multiple levels - interacting and influencing each other. Both are modulated by psychosocial factors including fears, beliefs, and goals, and are served by overlapping neural substrates. One major contributing factor in the development and maintenance of chronic pain is threat learning, with pain as an emotionally-salient threat – or stressor. Here, we argue that threat learning is a central mechanism and contributor, mediating the relationship between stress and chronic pain. We review the state of the art on (mal)adaptive learning in chronic pain, and on effects of stress and particularly cortisol on learning. We then provide a theoretical integration of how stress may affect chronic pain through its effect on threat learning. Prolonged stress, as may be experienced by patients with chronic pain, and its resulting changes in key brain networks modulating stress responses and threat learning, may further exacerbate these impairing effects on threat learning. We provide testable hypotheses and suggestions for how this integration may guide future research and clinical approaches in chronic pain

Volume and connectivity differences in brain networks associated with cognitive constructs of binge eating

Bulimia nervosa (BN) and binge eating disorder (BED) are characterized by episodes of eating large amounts of food while experiencing a loss of control. Recent studies suggest that the underlying causes of BN/BED consist of a complex system of environmental cues, atypical processing of food stimuli, altered behavioral responding, and structural/functional brain differences compared with healthy controls (HC). In this narrative review, we provide an integrative account of the brain networks associated with the three cognitive constructs most integral to BN and BED, namely increased reward sensitivity, decreased cognitive control, and altered negative affect and stress responding. We show altered activity in BED/BN within several brain networks, specifically in the striatum, insula, prefrontal cortex (PFC) and orbitofrontal cortex (OFC), and cingulate gyrus. Numerous key nodes in these networks also differ in volume and connectivity compared with HC. We provide suggestions for how this integration may guide future research into these brain networks and cognitive constructs

Stress-induced reliance on habitual behavior is moderated by cortisol reactivity

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