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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.

Previous experiments in the hippocampal CA1 area have shown that corticosterone can facilitate long-term potentiation (LTP) in a rapid non-genomic fashion, while the same hormone suppresses LTP that is induced several hours after hormone application. Here, we elaborated on this finding by examining whether corticosterone exerts opposite effects on LTP depending on the timing of hormone application in the dentate gyrus as well. Moreover, we tested rapid and delayed actions by corticosterone on ␤-adrenergic-dependent changes in LTP. Unlike the CA1 region, our in vitro field potential recordings show that rapid effects of corticosterone do not influence LTP induced by mild tetanization in the hippocampal dentate gyrus, unless GABA A receptors are blocked. In contrast, the ␤-adrenergic agonist isoproterenol does initiate a slow-onset, limited amount of potentiation. When corticosterone was applied concurrently with isoproterenol, a further enhancement of synaptic strength was identified, especially during the early stage of potentiation. Yet, treatment with corticosterone several hours in advance of isoproterenol fully prevented any effect of isoproterenol on LTP. This emphasizes that corticosterone can regulate ␤-adrenergic modulation of synaptic plasticity in opposite directions, depending on the timing of hormone application.

The rat basolateral amygdala is important for emotional learning; this is modulated by noradrenaline and corticosterone. We report that the b-adrenergic agonist isoproterenol markedly enhances synaptic plasticity induced in the basolateral amygdala by a weak stimulation paradigm but is ineffective with stronger protocols. Simultaneous application of corticosterone gradually reversed the facilitatory effect of isoproterenol. When corticosterone was briefly applied several hours prior to isoproterenol, facilitatory effects of the b-agonist were entirely suppressed. This suggests that in the basolateral amygdala, b-adrenergic influences promote synaptic plasticity; this is gradually normalized by corticosterone, preventing the network from overshooting.The amygdala is crucially involved in the modulation of emotional memory (Cahill and McGaugh 1998;LeDoux 2000;McGaugh 2004;Richter-Levin 2004), as clearly demonstrated in the animal model of fear conditioning (LeDoux et al. 1990;Romanski et al. 1993;Rogan et al. 1997;Nader et al. 2001;Blair et al. 2003). It was also proposed that the amygdala-that is, the basolateral nucleus (BLA)-can modulate memory-related processes in other brain regions, e.g., the hippocampus (McGaugh et al. 1996;Akirav and Richter-Levin 2002;Kim and Diamond 2002;Pare 2003; RichterLevin and Akirav 2003;Roozendaal 2003;Richter-Levin 2004;Roozendaal et al. 2006a); thus, memory traces constructed in the hippocampus that are ''emotionally tagged'' have a competitive advantage for retention (Richter-Levin and Akirav 2003;Diamond et al. 2005;Vouimba et al. 2007).Within the BLA, multiple neuromodulatory systems influence memory, including the noradrenergic and glucocorticoid systems (Quirarte et al. 1997;Roozendaal 2003;Roozendaal et al. 2006a). Animal behavioral studies suggested that noradrenergic activity within the BLA plays a central role in mediating a memoryenhancing effect, while glucocortoid receptor (GR) activation exerts a ''permissive'' function (Roozendaal et al. 2002(Roozendaal et al. , 2006b). However, experiments in which the two hormones were not given concurrently showed that glucocorticoids may otherwise suppress the noradrenergic effect (Borrell et al. 1984). This suggests that the interactive hormonal functions affecting the memory systems are not always uniform.Support for this nonuniformity was recently obtained in the hippocampal DG (Pu et al. 2007). Corticosterone time-dependently modulated noradrenergic action on long-term potentiation (LTP), the best-described neurobiological substrate of learning and memory to date (Goosens and Maren 2002;Martin and Morris 2002;Morris 2003). Thus, b-adrenergic facilitation of LTP was accelerated if corticosterone was coapplied with the b-agonist isoproterenol, but suppressed if corticosterone was transiently applied several hours before the b-agonist (Pu et al. 2007). In view of the behavioral observations that b-agonists and glucocorticoids both affect memory processes involving the BLA (Roozendaal et al. 2002), we here investigated the time...

The defects and phase segregation in perovskite will significantly reduce the performance and stability of perovskite solar cells (PSCs). In this work, a deformable coumarin is employed as a multifunctional additive for formamidinium–cesium (FA‐Cs) perovskite. During the annealing process of perovskite, the partial decomposition of coumarin passivates the Pb2+, iodine, and organic cation defects. Additionally, coumarin can affect colloidal size distributions, resulting in relatively large grain size and good crystallinity of target perovskite film. Hence, the carrier extraction/transport can be promoted, trap‐assisted recombination is reduced, and energy levels are optimized in target perovskite films. Furthermore, the coumarin treatment can significantly release residual stress. As a result, the champion power conversion efficiencies (PCEs) of 23.18% and 24.14% are obtained for Br‐rich (FA0.88Cs0.12PbI2.64Br0.36) and Br‐poor (FA0.96Cs0.04PbI2.8Br0.12) based devices, respectively. The flexible PSCs based on Br‐poor perovskite exhibit an excellent PCE of 23.13%, one of the highest values for flexible PSCs reported to date. Due to the inhibition of phase segregation, the target devices exhibit excellent thermal and light stability. This work provides new insights into the additive engineering of passivating defects, stress relief, and inhibition of phase segregation of perovskite films, offering a reliable method to develop state‐of‐the‐art solar cells.

The quality of the perovskite absorption layer is critical for the high efficiency and long‐term stability of perovskite solar cells (PSCs). The inhomogeneity due to local lattice mismatch causes severe residual strain in low‐quality perovskite films, which greatly limits the availability of high‐performance PSCs. In this study, a multi‐active‐site potassium salt, pemirolast potassium (PP), is added to perovskite films to improve carrier dynamics and release residual stress. X‐ray photoelectron spectroscopy (XPS) and Fourier‐transform infrared spectroscopy (FTIR) measurements suggest that the proposed multifunctional additive bonds with uncoordinated Pb2+ through the carbonyl group/tetrazole N and passivated I atom defects. Moreover, the residual stress release is effective from the surface to the entire perovskite layer, and carrier extraction/transport is promoted in PP‐modified perovskite films. As a result, a champion power conversion efficiency (PCE) of 23.06% with an ultra‐high fill factor (FF) of 84.36% is achieved in the PP‐modified device, which ranks among the best in formamidinium‐cesium (FACs) PSCs. In addition, the PP‐modified device exhibits excellent thermal stability due to the inhibited phase separation. This work provides a reliable way to improve the efficiency and stability of PSCs by releasing residual stress in perovskite films through additive engineering.