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Graphs representing group means for Session 2 recognition memory tasks. For both words and pictures, main effects of dose were found (Fs 3.21). Error bars represent SEM.
Source publication
In a test of the effects of cortisol on emotional memory, 90 men were orally administered placebo or 20 or 40 mg cortisol and presented with emotionally arousing and neutral stimuli. On memory tests administered within 1 hr of stimulus presentation, cortisol elevations caused a reduction in the number of errors committed on free-recall tasks. Two e...
Contexts in source publication
Context 1
... picture recognition memory at Session 2, a main effect of dose on sensitivity was found, F(2, 78) 6.37, p .01, but a Dose Stimulus Valence interaction was not found, F(2, 78) 0.08, ns (see Figure 3). The predicted quadratic trend was found across stimulus valence, F quadratic 6.58, p .02. ...
Context 2
... no Dose Stimulus Valence interaction emerged, F(2, 78) 1.06, ns. The predicted quadratic trend was found across Stimulus Valence, F quadratic 5.8, p .05 (see Figure 3). Across negative and neutral words, the 20-mg group performed better than the placebo group, t(54) 2.15, p .05 (effect size: d 0.57), and marginally significantly better than the 40-mg group, t(55) 1.91, p .06. ...
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Citations
... A second crucial factor is the duration of the stressful event, with different effects observed between short episodes (acute stress) or repetitive ones (chronic stress), the latter often contributing to the development of pathological conditions. Additionally, the phase of memory to which the stressful event is related plays a pivotal role; while stress tends to impair working memory, generally leads to consolidation benefits and memory recall damage (Abercrombie et al., 2003;Bahari et al., 2018;De Quervain et al., 2000;Joëls et al., 2011;Kuhlmann et al., 2005;Roozendaal, 2002;Shields et al., 2016a). According to the meta-analysis of Shields et al. (2017) when stress occurred prior to or during encoding it impaired memory, unless both the delay between the stressor and encoding was very short and the study materials were directly related to the stressor. ...
Understanding the impact of stress on cognitive processes, particularly decision-making, is crucial as it underpins behaviors essential for survival. However, research in this domain has yielded disparate results, with inconsistencies evident across stress-induction paradigms and drug administration protocols designed to investigate specific stress pathways or neuromodulators. Building upon empirical studies, this research identifies a multifaceted matrix of variables contributing to the divergent findings. This matrix encompasses factors such as the temporal proximity between stressors and decision tasks, the nature of stressors and decision contexts, individual characteristics including psychobiological profiles and affective states at the time of decision-making and even cultural influences. In response to these complexities, we propose a comprehensive model that integrates these relevant factors and their intricate interplay to elucidate the mechanisms governing decision-making during stressful events. By synthesizing these insights, our model not only refines existing paradigms but also provides a framework for future study designs, offering avenues for theoretical advancements and translational developments in the field of stress's impact on cognitive functions. This research contributes to a deeper understanding of the nuanced relationship between stress and decision-making, ultimately advancing our knowledge of cognitive processes under challenging conditions.
... Nonetheless, research often prioritizes male participants, emphasizing the need to elucidate the role of sex hormones in fear extinction [124,129,130]. The HPA, which is responsible for stress-induced activation and the release of glucocorticoids, plays a significant role in influencing cognitive processes, including the effects of stress and cortisol on memory, especially for emotional material, as consistently demonstrated in research [98,131]. A thorough understanding of cortisol, sex hormones, and emotional memory's interplay is pivotal, holding promise in enhancing our comprehension of stress-related disorders and refining therapeutic strategies. ...
Fear extinction is a phenomenon that involves a gradual reduction in conditioned fear responses through repeated exposure to fear-inducing cues. Functional brain connectivity assessments , such as functional magnetic resonance imaging (fMRI), provide valuable insights into how brain regions communicate during these processes. Stress, a ubiquitous aspect of life, influences fear learning and extinction by changing the activity of the amygdala, prefrontal cortex, and hippocampus, leading to enhanced fear responses and/or impaired extinction. Glucocorticoid receptors (GRs) are key to the stress response and show a dual function in fear regulation: while they enhance the consolidation of fear memories, they also facilitate extinction. Accordingly, GR dysregulation is associated with anxiety and mood disorders. Recent advancements in cognitive neuroscience underscore the need for a comprehensive understanding that integrates perspectives from the molecular, cellular, and systems levels. In particular, neuropharmacology provides valuable insights into neurotrans-mitter and receptor systems, aiding the investigation of mechanisms underlying fear regulation and potential therapeutic targets. A notable player in this context is cortisol, a key stress hormone, which significantly influences both fear memory reconsolidation and extinction processes. Gaining a thorough understanding of these intricate interactions has implications in terms of addressing psychiatric disorders related to stress. This review sheds light on the complex interactions between cognitive processes, emotions, and their neural bases. In this endeavor, our aim is to reshape the comprehension of fear, stress, and their implications for emotional well-being, ultimately aiding in the development of therapeutic interventions.
... On each trial, participants viewed an object and were asked to select which of four scenes was paired with the object at encoding (Fig. 1C). Participants selected the correctly paired scene more often than chance (chance ¼ 0.25; mean proportion correct ¼ 0. Prior work has demonstrated that subjective affect can modulate cortisol effects on memory (Abercrombie et al., 2003). Thus, we examined whether memory was affected by subjective arousal differently under hydrocortisone versus placebo. ...
... Although cortisol administration before encoding did not impact memory overall, cortisol enhanced associative memory for participants who experienced greater subjective arousal (across both the Emotional and Neutral blocks). This arousal-specific enhancement of memories under stress has been demonstrated previously and highlights the importance of assessing subjective arousal when measuring stress effects on memory (Buchanan and Lovallo, 2001;Abercrombie et al., 2003Abercrombie et al., , 2006Goldfarb et al., 2019), rather than focusing on broadly arousing versus nonarousing stimulus categories. However, most prior work focused on negative affect (Abercrombie et al., Goldfarb et al., 2019). ...
... This finding adds to burgeoning literature that acute stress promotes positive emotional memories (Kamp et al., 2019), and accords with work outside the stress domain demonstrating that positive emotion can bolster associative memory (Madan et al., 2019). Relatedly, cortisol amplified the perceived emotional salience of memoranda, with participants less likely to rate associations as "neutral" (similar to Abercrombie et al., 2003). Importantly, this cortisol-induced shift in affect valuation was specific to the encoded associations, and did not reflect a broader hydrocortisone-induced change in affect. ...
Stress can powerfully influence episodic memory, often enhancing memory encoding for emotionally salient information. These stress-induced memory enhancements stand at odds with demonstrations that stress and the stress-related hormone cortisol can negatively affect the hippocampus, a brain region important for episodic memory encoding. To resolve this apparent conflict and determine whether and how the hippocampus supports memory encoding under cortisol, we combined behavioral assays of associative memory, high-resolution functional magnetic resonance imaging (fMRI), and pharmacological manipulation of cortisol in a within-participant, double-blinded procedure (in both sexes). Behaviorally, hydrocortisone promoted the encoding of subjectively arousing, positive associative memories. Neurally, hydrocortisone led to enhanced functional connectivity between hippocampal subregions, which predicted subsequent memory enhancements for emotional associations. Cortisol also modified the relationship between hippocampal representations and associative memory: whereas hippocampal signatures of distinctiveness predicted memory under placebo, relative integration predicted memory under cortisol. Together, these data provide novel evidence that the human hippocampus contains the necessary machinery to support emotional associative memory enhancements under cortisol.
Significance Statement
Our daily lives are filled with stressful events, which powerfully shape the way we form episodic memories. For example, stress and stress-related hormones can enhance our memory for emotional events. However, the mechanisms underlying these memory benefits are unclear. In the current study, we combined functional neuroimaging, behavioral tests of memory, and double-blind, placebo-controlled hydrocortisone administration to uncover the effects of the stress-related hormone cortisol on the function of the human hippocampus, a brain region important for episodic memory. We identified novel ways in which cortisol can enhance hippocampal function to promote emotional memories, highlighting the adaptive role of cortisol in shaping memory formation.
... Second, the time of the day in which eGCs are administered appears to be an important determinant of their cognitive effects. Specifically, administration of modest doses (i.e., hydrocortisone 20-40 mg) before cognitive testing in the afternoon results in mild memory enhancement [240], whereas a morning administration (a time in which GRs are already partially saturated by higher endogenous cortisol levels) is associated with memory impairment [118], likely due to the oversaturation of GRs [241]. ...
... Regarding cognitive functioning, the relation between SIAGC dose and memory typically follows an inverted U-shaped function [241,266], facilitating delayed memory retrieval at a threshold dose of 20 mg/day of hydrocortisone (which mirrors the physiological cortisol increases during mild stress), with higher doses resulting in impaired cognitive function [241]. ...
... Regarding cognitive functioning, the relation between SIAGC dose and memory typically follows an inverted U-shaped function [241,266], facilitating delayed memory retrieval at a threshold dose of 20 mg/day of hydrocortisone (which mirrors the physiological cortisol increases during mild stress), with higher doses resulting in impaired cognitive function [241]. ...
Purpose:
The hypothalamic-pituitary-adrenal (HPA) axis exerts many actions on the central nervous system (CNS) aside from stress regulation. Glucocorticoids (GCs) play an important role in affecting several cognitive functions through the effects on both glucocorticoid (GR) and mineralocorticoid receptors (MR). In this review, we aim to unravel the spectrum of cognitive dysfunction secondary to derangement of circulating levels of endogenous and exogenous glucocorticoids.
Methods:
All relevant human prospective and retrospective studies published up to 2022 in PubMed reporting information on HPA disorders, GCs, and cognition were included.
Results:
Cognitive impairment is commonly found in GC-related disorders. The main brain areas affected are the hippocampus and pre-frontal cortex, with memory being the most affected domain. Disease duration, circadian rhythm disruption, circulating GCs levels, and unbalanced MR/GR activation are all risk factors for cognitive decline in these patients, albeit with conflicting data among different conditions. Lack of normalization of cognitive dysfunction after treatment is potentially attributable to GC-dependent structural brain alterations, which can persist even after long-term remission.
Conclusion:
The recognition of cognitive deficits in patients with GC-related disorders is challenging, often delayed, or mistaken. Prompt recognition and treatment of underlying disease may be important to avoid a long-lasting impact on GC-sensitive areas of the brain. However, the resolution of hormonal imbalance is not always followed by complete recovery, suggesting irreversible adverse effects on the CNS, for which there are no specific treatments. Further studies are needed to find the mechanisms involved, which may eventually be targeted for treatment strategies.
... The fear extinction phase was scheduled 72 h after fear conditioning, with study drug (HC 25 mg, DCS 50 mg, or placebo) administered 1 h prior to the fear extinction phase. The 25 mg HC dose was selected based on findings that 20-25 mg of HC was effective for facilitating memory, but that higher doses (i.e., 40 mg) were not [37,38]. The 50 mg DCS dose was selected since it was the most commonly used dose in prior clinical trials and previously determined to be effective in enhancing extinction learning [39][40][41]. ...
Fear extinction underlies prolonged exposure, one of the most well-studied treatments for posttraumatic stress disorder (PTSD). There has been increased interest in exploring pharmacological agents to enhance fear extinction learning in humans and their potential as adjuncts to PE. The objective of such adjuncts is to augment the clinical impact of PE on the durability and magnitude of symptom reduction. In this study, we examined whether hydrocortisone (HC), a corticosteroid, and D-Cycloserine (DCS), an N-methyl-D-aspartate receptor partial agonist, enhance fear extinction learning and consolidation in individuals with PTSD. In a double-blind placebo-controlled 3-group experimental design, 90 individuals with full or subsyndromal PTSD underwent fear conditioning with stimuli that were paired (CS+) or unpaired (CS−) with shock. Extinction learning occurred 72 h later and extinction retention was tested one week after extinction. HC 25 mg, DCS 50 mg or placebo was administered one hour prior to extinction learning. During extinction learning, the DCS and HC groups showed a reduced differential CS+/CS− skin conductance response (SCR) compared to placebo (b = −0.19, CI = −0.01 to −37, p = 0.042 and b = −0.25, CI = −08 to −0.43, p = 0.005, respectively). A nonsignificant trend for a lower differential CS+/CS− SCR in the DCS group, compared to placebo, (b = −0.25, CI = 0.04 to −0.55, p = 0.089) was observed at retention testing, one week later. A single dose of HC and DCS facilitated fear extinction learning in participants with PTSD symptoms. While clinical implications have yet to be determined, our findings suggest that glucocorticoids and NMDA agonists hold promise for facilitating extinction learning in PTSD.
... On the other hand, acutely elevated GCs can either enhance(114,(134)(135)(136)(137)(138) or impair memory depending on several factors, including but not limited to, the time of day of cognitive testing, the stage at which a stressor is applied (i.e., at encoding, consolidation or retrieval), and the dose of GC administered(139,140). ...
Sleep is a critical biological process, essential for cognitive well-being. Neuroscientific literature suggests there are mechanistic relations between sleep disruption and memory deficits, and that varying concentrations of cortisol may play an important role in mediating those relations. Patients with Addison’s disease (AD) experience consistent and predictable periods of sub- and supra-physiological cortisol concentrations due to lifelong glucocorticoid replacement therapy, and they frequently report disrupted sleep and impaired memory. These disruptions and impairments may be related to the failure of replacement regimens to restore a normal circadian rhythm of cortisol secretion. Available data provides support for existing theoretical frameworks which postulate that in AD and other neuroendocrine, neurological, or psychiatric disorders, disrupted sleep is an important biological mechanism that underlies, at least partially, the memory impairments that patients frequently report experiencing. Given the literature linking sleep disruption and cognitive impairment in AD, future initiatives should aim to improve patients’ cognitive performance (and, indeed, their overall quality of life) by prioritizing and optimizing sleep. This review summarizes the literature on sleep and cognition in AD, and the role that cortisol concentrations play in the relationship between the two.
... It has often been documented that patients with AI frequently suffer from a reduced quality of life and sleep [9]. The influence of glucocorticoid dose was also investigated, with an inverse Ushaped distribution between glucocorticoids and memory performance [10]. It was found that moderate doses enhance consolidation processes, whereas lower or higher doses are typically less effective or even induce memory impairment [11]. ...
PurposePatients with adrenal insufficiency are usually treated with conventional hydrocortisone replacement therapy which fails to mimic the circadian rhythm of cortisol secretion. Dual-release hydrocortisone (DR-HC) resembles the daily normal cortisol profile improving metabolic parameters and quality of life. However, currently little is known about its impact on cognitive function. Aim of this study was to evaluate cognitive function and well-being in DR-HC treated patients compared to healthy controls and conventional HC treatment.Methods
Twenty adults with adrenal insufficiency treated with DR-HC (Plenadren®) underwent 10 neuropsychological tests, evaluating cognitive functions. Furthermore, demographic data, quality of life, symptoms of depression, and quality of sleep were evaluated by well-established questionnaires. Patients were compared by diagnosis (PAI/SAI) and dose (≥20 mg). In addition, eighteen DR-HC treated adults were compared to eighteen matched conventionally treated adults.ResultsWith respect to diagnosis patients with PAI performed significantly better on intellectual abilities (p = 0.038) and on executive functioning (p = 0.026) and reported a significant longer time to fall asleep (p = 0.026). Regarding DR-HC dosage, there were no significant differences in cognitive functions. Patients on high dose reported a better subjective quality of sleep (p = 0.028) than patients on low dose. In comparison to conventional HC treatment, patients with DR-HC tended to show better results in executive functioning (p = 0.099).Conclusion
Patients with PAI reached better results in several cognitive functions and had a worse quality of sleep than patients with SAI. Our data suggest a positive impact of DR-HC on quality of sleep. DR-HC may be better for executive functioning.
... Les patients dépressifs montrent des difficultés particulières dans les tâches mnésiques nécessitant un effort, comme l'apprentissage d'une liste et son rappel (Basso and Bornstein, 1999b). De nombreuses études révèlent une diminution dans la capacité à acquérir de nouvelles informations en lien avec l'existence de pensées négatives/pessimistes qui viennent perturber les fonctions mnésiques (Cronholm and Ottosson, 1961;Stromgren, 1977 Cette classification associe chaque type d'opération à une structure cérébrale impliquée dans l'encodage des informations (d'après Squire, 1992Squire, , 2004 Figure 8 : Classification dichotomique des systèmes de mémoire à long terme Cette classification associe chaque type d'opération à une structure cérébrale impliquée dans l'encodage des informations (Squire, 1992(Squire, , 2004 suit, là aussi, un profile en U inversé (Abercrombie et al., 2003;Domes et al., 2005;Schilling et al., 2013). D'un point de vue qualitatif, le stress module la réponse comportementale favorisant la mise en place d'associations de type stimulus-réponse, dépendant du striatum, au détriment d'associations de type stimulus-stimulus (spatiales), dépendant de l'HPC . ...
Le stress chronique est un phénomène universel qui concerne toutes les strates de la société, quels que soient l’âge, le sexe, le milieu social, les origines culturelles et géographiques. Néanmoins la vulnérabilité est variable selon l’âge d’exposition. Il est aujourd’hui avéré qu’une exposition chronique à un stress ou bien une exposition à un stress aigu intense chez l’enfant, voire même pendant la période périnatale, peut avoir des conséquences dramatiques sur le développement cérébral et peut engendrer un certain nombre de pathologies neuropsychiatriques plus tard au cours de la vie. Néanmoins, une plus forte résistance et une capacité de résilience apparaît à l’âge adulte se caractérisant notamment par une adaptabilité et la possibilité de retourner rapidement à un état initial après une exposition au stress. Toutefois, des travaux récents suggèrent qu’une seconde phase de vulnérabilité apparait en milieu de vie, période charnière durant laquelle certaines structures du système limbique commencent peu à peu à décliner. L’objectif de cette thèse a été ainsi dans un premier temps de mieux caractériser la nature des perturbations somatiques à court terme et des déficits comportementaux à long terme qui apparaissent suite à un stress chronique durant cette période charnière au cours de laquelle s’installe une vulnérabilité accrue aux stress. Pour répondre à cette première problématique, le modèle de stress chronique léger et imprédictible mis au point chez la souris a été utilisé. Les impacts à court terme ont été déterminés en analysant les troubles somatiques et endocriniens, puis ceux à long-terme (chez le sujet âgé), ont été déterminés en analysant les troubles comportementaux anxieux, dépressifs et cognitifs, caractéristiques du syndrome de stress. D’autre part, il s’agissait d’identifier les réorganisations épigénétiques associés au vieillissement et au stress chronique ayant eu lieu en milieu de vie. Nous nous sommes concentrés sur les perturbations de la marque permissive H3K9ac et la marque répressive H3K27me3 en fonction du vieillissement et du stress chronique à long terme. Enfin, une approche pharmacologique a été utilisée pour évaluer l’impact d’un traitement ciblant ces mécanismes épigénétiques sur les déficits comportementaux. Un traitement chronique de 3 semaines à base de butyrate de sodium (NaB) qui est un iHDAC, a été administré aux animaux après la phase de stress chronique, puis les évaluations comportementales ont été réalisé à long terme, chez les sujets âgés.
... The intrinsic nature of the decision that has to be made is likely to be associated with a more acute cortisol response, whereas a pre-existing state, which may or may not be associated with the context of the financial risk to be taken, will result in a more prolonged cortisol reaction which may also influence that decision in a manner that is different from more acute or short-term cortisol responses . Acute administration of cortisol in other contexts increases the arousal response to stimuli, as well as enhancing the consolidation of memories of adverse events whilst reducing their recall (Abercrombie et al., 2003(Abercrombie et al., , 2005Wirth et al., 2011;Wolf et al., 2016). There are similar indicators in the brain: the reaction of the amygdala (which contains profuse glucocorticoid receptors) to facial expression changes with time, an effect which has been related to its connections with the medial frontal cortex (Henckens et al., 2010). ...
Hormones exert powerful, but covert, effects on financial decision-making. These vary according to the context of the decision, the type of decision being made and features of the individual making that decision. There are differences, for example, between rapid decisions made under duress (e.g. trading) and more deliberate ones made cooperatively (e.g. management) and those made by trained professional or financial management in everyday life. This chapter focusses mainly on acute decisions. Most studies have been made on males, who have dominated professional finance. Financial decisions involve both cognition and emotion, though the two are not clearly separable. They involve both risk and reward evaluations, and hormones, particularly testosterone, cortisol and oxytocin, influence both. The rewarding function of money has to be learned, and this involves areas of the brain such as the amygdala, which are heavily influenced by steroid hormones. Decisions are influenced not only by reward (utility) but by emotions (e.g. ‘framing’). Stress, and associated levels of cortisol, can impair attention and risk assessment, and levels alter in response to uncertainty; however more prolonged increases may have different effects on risk appetite and impulsivity. Testosterone enhances competitiveness, aggression, risk appetite and optimism in finance as it does in its major role in reproduction. Testosterone levels are also sensitive to winning or losing, and this may affect subsequent decisions. In females, phases of the menstrual cycle alter risk appetite, which is maximal at midcycle. Oxytocin administration increases trust, an essential ingredient of financial transactions. Within each individual, it is the pattern of these hormones, and how they change, that determines the influence they will have on financial decisions, which should not be underestimated, though their roles have received little consideration in the world of finance.
... It has been shown that pharmacological stimulation of stress hormones including glucocorticoids, vasopressin, corticotropin-releasing factor (CRF) and adrenocorticotropin releasing hormone (ACTH) shortly after training on a variety of emotional arousing learning tasks leads to better performance when subjects are retestedstress-free (Bohus et al., 1978;De Kloet et al., 1999;de Wied et al., 1976;Roozendaal et al., 2007;Schwabe et al., 2012). Moreover, selective blockade of glucocorticoid receptors immediately after training impairs memory performance of inhibitory avoidance (Oitzl and de Kloet, 1992), and elevated cortisol levels predict better memory for emotionally charged material when subjects are presented with stressful situations post-learning (Abercrombie et al., 2003(Abercrombie et al., , 2006Cahill et al., 2003;Smeets et al., 2008). This said, the relationship between activation of stress hormones and memory consolidation appears to follow an inverted-U function (Abercrombie et al., 2003;McGaugh, 2013) as there is evidence that high levels of corticosterone can lead to memory impairments (Diamond et al., 2004;Schwabe et al., 2010;Smeets et al., 2008;Trammell and Clore, 2014). ...
... Moreover, selective blockade of glucocorticoid receptors immediately after training impairs memory performance of inhibitory avoidance (Oitzl and de Kloet, 1992), and elevated cortisol levels predict better memory for emotionally charged material when subjects are presented with stressful situations post-learning (Abercrombie et al., 2003(Abercrombie et al., , 2006Cahill et al., 2003;Smeets et al., 2008). This said, the relationship between activation of stress hormones and memory consolidation appears to follow an inverted-U function (Abercrombie et al., 2003;McGaugh, 2013) as there is evidence that high levels of corticosterone can lead to memory impairments (Diamond et al., 2004;Schwabe et al., 2010;Smeets et al., 2008;Trammell and Clore, 2014). ...
It is well established that learning and memory are central to substance dependence. This paper specifically reviews the effect of opioid withdrawal on memory consolidation. Although there is evidence that opioid withdrawal can interfere with initial acquisition and retrieval of older memories, there are several reasons to postulate a facilitatory action on the consolidation of newly acquired memories. In fact, there is substantial evidence that memory consolidation is facilitated by the release of stress hormones, that it requires the activation of the amygdala, central noradrenergic and cholinergic pathways, and that it involves long-term potentiation. This review highlights evidence that very similar neurobiological processes are activated during opioid withdrawal, and summarizes the results of a study which found that naltrexone-precipitated withdrawal enhanced consolidation of object memory in morphine-maintained rats. From this neurocognitive perspective, therefore, opioid use may escalate during the addiction cycle in part because memories of stimuli and actions experienced during withdrawal are strengthened.
