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

The impairing effect of acute stress on suppression-induced forgetting of future fears and its moderation by working memory capacity

Unwanted imaginations of future fears can, to some extent, be avoided. This is achieved by control mechanisms similar to those engaged to suppress and forget unwanted memories. Suppression-induced forgetting relies on the executive control network, whose functioning is impaired after exposure to acute stress. This study investigates whether acute stress affects the ability to intentionally control future fears and, furthermore, whether individual differences in executive control predict a susceptibility to these effects. The study ran over two consecutive days. On day 1, the working memory capacity of one hundred participants was assessed. Thereafter, participants provided descriptions and details of fearful episodes that they imagined might happen in their future. On day 2, participants were exposed to either the stress or no-stress version of the Maastricht Acute Stress Test, after which participants performed the Imagine/No-Imagine task. Here, participants repeatedly imagined some future fears and suppressed imaginings of others. Results demonstrated that, in unstressed participants, suppression successfully induced forgetting of the episodes’ details compared to a baseline condition. However, anxiety toward these events did not differ. Acute stress was found to selectively impair suppression-induced forgetting and, further, this effect was moderated by working memory capacity. Specifically, lower working memory predicted a susceptibility to these detrimental effects. These findings provide novel insights into conditions under which our capacity to actively control future fears is reduced, which may have considerable implications for understanding stress-related psychopathologies and symptomatologies characterized by unwanted apprehensive thoughts

Orienting melt to produce on lab-microscale high performance and ultra thin foils

Efficient molecular orientation of polymers in the melt-or solution state requires concentric contraction flows, which result in single or multi-filament fiber shaped products. Directed molecular orientation in pipes, sheets, foils and films, like strip bi-axially, planar or tri-axial, are difficult to achieve and require complex multi-stage processing often supported by the addition of extra external magnetic, electric, or temperature gradient fields that put constraints to the materials to be processed. Here we aim at a simple continuous process to produce uni-axially oriented foils, by designing a special die in a standard miniaturized laboratory scale film casting process. The internal of the die consist of a fiber forming, and a fiber fusing part. The specific design of the fiber forming part allows the combination of the fibers formed, without them crossing, into a line that forms a sheet. Flow in the total volume around the slit ends up in molecularly oriented flow inside the slit. To preserve orientation, an air gap extrusion process follows the exiting slit flow, to allow for a strong draw down under high melt stress. Small air-gaps and a cold cooling nose, combined with a supporting carrying film, make the total process easy, clean and cheap, and the products unique. We will demonstrate that, mounted on the miniature Xplore MC 15 lab compounder, the device is able to produce not only high performance fully oriented foils based on a thermotropic liquid crystalline polyester (Vectra), but also extremely thin foils of polyamides and polyesters. In the last application, the melt orientation is used only to temporary obtain a high melt strength that allows a high draw-ability in the air gap.</p

Mitigating the negative effects of retrieval stress on memory: an arousal reappraisal intervention

In a preregistered experiment, we examined the efficacy of arousal reappraisal as an intervention for reducing the negative effects of stress at retrieval on memory. Participants (N = 177) were semi-randomly assigned to one of three conditions: a Stress-intervention condition, a Stress-placebo condition, and a No-stress-placebo control condition. Participants viewed four images of complex, mildly negatively valenced scenes. One day later, they received an arousal reappraisal intervention or placebo before exposure to a laboratory stressor (or a control version for the No-stress condition). Participants were then tested on their memory of the images using a free recall instruction and multiple-choice recognition questions. As expected, negative affect and blood pressure increased for the stress conditions but not the control condition. Contrary to our hypotheses, memory performance did not statistically significant differ between the Stress-placebo condition and the No-stress-placebo control condition, indicating a lack of negative effects of acute retrieval stress on memory. Furthermore, we also found no statistically significant differences between the Stress-intervention condition and Stress-placebo condition in terms of memory performance, suggesting that the intervention did not assist with enhancing memory. We integrate interpretations of the findings from this study with a discussion of avenues for future research in this area.status: publishe

Dopaminergic and noradrenergic modulation of stress-induced alterations in brain activation associated with goal-directed behaviour

BACKGROUND: Acute stress is thought to reduce goal-directed behaviour, an effect purportedly associated with stress-induced release of catecholamines. In contrast, experimentally increased systemic catecholamine levels have been shown to increase goal-directed behaviour. Whether experimentally increased catecholamine function can modulate stress-induced reductions in goal-directed behaviour and its neural substrates, is currently unknown. AIM: To assess whether and how experimentally induced increases in dopamine and noradrenaline contribute to the acute stress effects on goal-directed behaviour and associated brain activation. METHODS: One hundred participants underwent a stress induction protocol (Maastricht acute stress test; MAST) or a control procedure and received methylphenidate (MPH) (40 mg, oral) or placebo according to a 2 × 2 between-subjects design. In a well-established instrumental learning paradigm, participants learnt stimulus–response–outcome associations, after which rewards were selectively devalued. Participants’ brain activation and associated goal-directed behaviour were assessed in a magnetic resonance imaging scanner at peak cortisol/MPH concentrations. RESULTS: The MAST and MPH increased physiological measures of stress (salivary cortisol and blood pressure), but only MAST increased subjective measures of stress. MPH modulated stress effects on activation of brain areas associated with goal-directed behaviour, including insula, putamen, amygdala, medial prefrontal cortex, frontal pole and orbitofrontal cortex. However, MPH did not modulate the tendency of stress to induce a reduction in goal-directed behaviour. CONCLUSION: Our neuroimaging data suggest that MPH-induced increases in dopamine and noradrenaline reverse stress-induced changes in key brain regions associated with goal-directed behaviour, while behavioural effects were absent. These effects may be relevant for preventing stress-induced maladaptive behaviour like in addiction or binge eating disorder

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

Stress impairs intentional memory control through altered theta oscillations in lateral parietal cortex

Accumulating evidence suggests that forgetting is not necessarily a passive process but that we can, to some extent, actively control what we remember and what we forget. Although this intentional control of memory has potentially far-reaching implications, the factors that influence our capacity to intentionally control our memory are largely unknown. Here, we tested whether acute stress may disrupt the intentional control of memory and, if so, through which neural mechanism. We exposed healthy men and women to a stress (n=27) or control (n=26) procedure before they aimed repeatedly to retrieve some previously learned cue-target pairs and to actively suppress others. While control participants showed reduced memory for supressed compared to baseline pairs in a subsequent memory test, this suppression-induced forgetting was completely abolished after stress. Using magnetoencephalography (MEG), we show that the reduced ability to suppress memories after stress is associated with altered theta activity in the inferior temporal cortex when the control process (retrieval or suppression) is triggered and in the lateral parietal cortex when control is exerted, with the latter being directly correlated with the stress hormone cortisol. Moreover, the suppression-induced forgetting was linked to altered connectivity between the hippocampus and right dorsolateral prefrontal cortex, which in turn was negatively correlated to stress-induced cortisol increases. These findings provide novel insights into conditions under which our capacity to actively control our memory breaks down and may have considerable implications for stress-related psychopathologies, such as posttraumatic stress disorder, that are characterized by unwanted memories of distressing events.Significance Statement: It is typically assumed that forgetting is a passive process that can hardly be controlled. There is, however, evidence that we may actively control, to some extent, what we remember and what we forget. This intentional memory control has considerable implications for mental disorders in which patients suffer from unwanted (e.g., traumatic) memories. Here, we demonstrate that the capacity to intentionally control our memory breaks down after stress. Using magnetoencephalography, we show that this stress-induced memory control deficit is linked to altered activity in the lateral parietal cortex and the connectivity between the hippocampus and right prefrontal cortex. These findings provide novel insights into conditions under which memory control fails and are highly relevant in the context of stress-related psychopathologies