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Stressed memories: How acute stress affects memory formation in humansHenckens, M.J.A.G.; Hermans, E.J.; Pu, Z.; Joëls, M.; Fernández, G. General rightsIt is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulationsIf you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: http://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. Stressful, aversive events are extremely well remembered. Such a declarative memory enhancement is evidently beneficial for survival, but the same mechanism may become maladaptive and culminate in mental diseases such as posttraumatic stress disorder (PTSD). Stress hormones are known to enhance postlearning consolidation of aversive memories but are also thought to have immediate effects on attentional, sensory, and mnemonic processes at memory formation. Despite their significance for our understanding of the etiology of stress-related mental disorders, effects of acute stress at memory formation, and their brain correlates at the system scale, remain elusive. Using an integrated experimental approach, we probed the neural correlates of memory formation while participants underwent a controlled stress induction procedure in a crossover design. Physiological (cortisol level, heart rate, and pupil dilation) and subjective measures confirmed acute stress. Remarkably, reduced hippocampal activation during encoding predicted stress-enhanced memory performance, both within and between participants. Stress, moreover, amplified early visual and inferior temporal responses, suggesting that hypervigilant processing goes along with enhanced inferior temporal information reduction to relay a higher proportion of taskrelevant information to the hippocampus. Thus, acute stress affects neural correlates of memory formation in an unexpected manner, the understanding of which may elucidate mechanisms underlying psychological trauma etiology.

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Stress has a powerful impact on memory. Corticosteroids, released in response to stress, are thought to mediate, at least in part, these effects by affecting neuronal plasticity in brain regions involved in memory formation, including the hippocampus and prefrontal cortex. Animal studies have delineated aspects of the underlying physiological mechanisms, revealing rapid, nongenomic effects facilitating synaptic plasticity, followed several hours later by a gene-mediated suppression of this plasticity. Here, we tested the hypothesis that corticosteroids would also rapidly upregulate and slowly downregulate brain regions critical for episodic memory formation in humans. To target rapid and slow effects of corticosteroids on neural processing associated with memory formation, we investigated 18 young, healthy men who received 20 mg hydrocortisone either 30 or 180 min before a memory encoding task in a double-blind, placebo-controlled, counter-balanced, crossover design. We used functional MRI to measure neural responses during these memory encoding sessions, which were separated by a month. Results revealed that corticosteroids' slow effects reduced both prefrontal and hippocampal responses, while no significant rapid actions of corticosteroids were observed. Thereby, this study provides initial evidence for dynamically changing corticosteroid effects on brain regions involved in memory formation in humans.