Cortisol-Induced Impairments of Working Memory Require Acute Sympathetic Activation

Section of Clinical and Health Psychology, University of Leiden, Leiden, Netherlands.
Behavioral Neuroscience (Impact Factor: 2.73). 03/2005; 119(1):98-103. DOI: 10.1037/0735-7044.119.1.98
Source: PubMed


The present study assessed whether the effects of cortisol on working memory depend on the level of adrenergic activity (as measured by sympathetic activation) during memory performance. After exposure to a psychosocial stress task, participants were divided into cortisol responders and nonresponders. Cortisol responders showed working memory impairments during the psychosocial stress phase, when cortisol and adrenergic activity were enhanced, whereas nonresponders did not. During recovery, however, when cortisol levels were elevated but adrenergic activity was normalized, working memory of responders did not differ from that of nonresponders. Among several stress measures, cortisol was the only significant predictor for working memory performance during stress. These findings suggest that adrenergic activation is essential for the impairing effects of stress-induced cortisol on working memory.

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    • "A second possible factor, cortisol, has also been linked to impairments in working memory (Elzinga & Roelofs, 2005; Lupien et al., 1999). Stress-induced cortisol release is a good candidate as a mediator of the observed impairments in working memory after stress. "
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    ABSTRACT: A large and growing body of research demonstrates the impact of psychological stress on working memory. However, the typical study approach tests the effects of a single biological or psychological factor on changes in working memory. The current study attempted to move beyond the standard single-factor assessment by examining the impact of 2 possible factors in stress-related working memory impairments. To this end, 60 participants completed a working memory task before and after either a psychological stressor writing task or a control writing task and completed measures of both cortisol and mind wandering. We also included a measure of state anxiety to examine the direct and indirect effect on working memory. We found that mind wandering mediated the relationship between state anxiety and working memory at the baseline measurement. This indirect relationship was moderated by cortisol, such that the impact of mind wandering on working memory increased as cortisol levels increased. No overall working memory impairment was observed following the stress manipulation, but increases in state anxiety and mind wandering were observed. State anxiety and mind wandering independently mediated the relationship between change in working memory and threat perception. The indirect paths resulted in opposing effects on working memory. Combined, the findings from this study suggest that cortisol enhances the impact of mind wandering on working memory, that state anxiety may not always result in stress-related working memory impairments, and that high working memory performance can protect against mind wandering. (PsycINFO Database Record (c) 2015 APA, all rights reserved).
    Emotion 06/2015; DOI:10.1037/emo0000096 · 3.88 Impact Factor
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    • "Working memory has been shown to depend on the dorsolateral prefrontal cortex (Carlson, 2010; Kandel et al., 1991; Gazzaniga et al., 2014). he prefrontal cortex is an area of particularly dense GR expression in the primate brain (Pryce, 2008; Sanchez et al., 2000), so GCs likely influence working memory by acting at receptors in this region. Also of note, as with memory consolidation and retrieval, the effects of GCs on working memory also depend on elevated norepinephrine in the amygdala (Elzinga and Roelofs, 2005). Notably, the impact of GCs on working memory once again seems to follow an inverted-U-shaped dose-response curve, but this curve is shifted to the left, so that smaller doses of GCs are sufficient to impair working memory compared to consolidation of episodic memory. "
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    ABSTRACT: Hormones have nuanced effects on learning and memory processes. The degree and direction of the effect (e.g., is memory impaired or enhanced?) depends on the dose, type and stage of memory, and type of material being learned, among other factors. This review will focus on two specific topics within the realm of effects of hormones on memory: (1) How glucocorticoids (the output hormones of the hypothalamic-pituitary-adrenal axis) affect long-term memory consolidation, retrieval, and working memory, with a focus on neural mechanisms and effects of emotion; and (2) How oxytocin affects memory, with emphasis on a speculative hypothesis that oxytocin might exert its myriad effects on human social cognition and behavior via impacts on more general cognitive processes. Oxytocin-glucocorticoid interactions will be briefly addressed. These effects of hormones on memory will also be considered from an evolutionary perspective.
    06/2015; 1(2). DOI:10.1007/s40750-014-0010-4
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    • "In contrast, as noted earlier, evidence from both rodents and humans suggests that glucocorticoid elevation can impair memory performance. In addition, in humans, this impairment has been seen with particular consistency for working memory as assessed with the Digit Span test (Elzinga and Roelofs, 2005; Schoofs et al., 2009; Vaz et al., 2011; Wolf et al., 2001 "
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    ABSTRACT: Individuals with classic congenital adrenal hyperplasia (CAH) experience impaired glucocorticoid production and are treated postnatally with glucocorticoids. Prior research with animals and other human populations indicates that glucocorticoids can influence memory, particularly working memory. We tested the hypothesis that children with CAH would show reduced working memory. Children in the United Kingdom, aged 7-11 years, with classical CAH (31 girls, 26 boys) were compared to their unaffected relatives (30 girls, 20 boys) on a test of working memory, the Digit Span test. Vocabulary was also assessed to measure verbal intelligence for control purposes. Children with CAH showed reduced working memory performance compared to controls, on both components of the Digit Span test: p=.008 for Digit Span Forward, and p=.027 for Digit Span Backward, and on a composite score, p=.004. These differences were of moderate size (d=.53 to .70). Similar differences were also seen in a subset of 23 matched pairs of children with CAH and their relatives (d=.78 to .92). There were no group differences on Vocabulary. Glucocorticoid abnormality, including treatment effects, could be responsible for the reduced Digit Span performance in children with CAH. Other factors related to CAH, such as salt-wasting crises, could also be involved. Additional research is needed to identify the cause of the memory reduction, which will help to determine if more rapid diagnosis or more precise glucocorticoid treatment would help prevent memory reduction. Educational interventions might also be considered for children with CAH. Copyright © 2014. Published by Elsevier Inc.
    Hormones and Behavior 12/2014; 67. DOI:10.1016/j.yhbeh.2014.11.014 · 4.63 Impact Factor
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