Stress- and treatment-induced elevations of cortisol levels associated with impaired declarative memory in healthy adults

Kirschbaum, Clemens; Wolf, Oliver T.; May, Mark A.; Wippich, Werner; Hellhammer, Dirk H.

doi:10.1016/0024-3205(96)00118-x

Cited by 727 publications

(510 citation statements)

References 29 publications

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“…Moreover, applying a within-subjects design, the present study was able to compare high GC-responders and low responders to the TSST. While this corroborates findings of possible positive correlations between stress-induced GC changes and declarative memory, our results appear to be in contrast to results reported by others who demonstrated a deterioration of memory performance in TSST responders (Kirschbaum et al, 1996;Wolf et al, 2001b;Takahashi et al, 2004;Elzinga and Roelofs, 2005). This different finding may be explained by the different memory functions tested or by the time of testing (morning vs. afternoon).…”

Section: Discussionsupporting

confidence: 83%

“…Among these studies, most have employed exogenous administration of GCs. Results from these studies were predominantly showing enhanced memory consolidation, whereas studies focusing on memory retrieval processes found impaired retrieval due to increased GC levels (Kirschbaum et al, 1996;de Quervain et al, 2000;Buchanan and Lovallo, 2001;Wolf et al, 2001a;Lupien et al, 2002;Monk and Nelson, 2002;de Quervain et al, 2003;Tops et al, 2003;Maheu et al, 2005b;Buchanan et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

“…In studies using the TSST or similar paradigms, psychosocial stress mostly resulted in impaired memory retreival (Kirschbaum et al, 1996;Lupien et al, 1997;Wolf et al, 2001b;Kuhlmann et al, 2005b), with some studies showing enhanced consolidation (Abercrombie et al, 2006;Beckner et al, 2006). Importantly though, individual cortisol responses due to stress may vary greatly (Kirschbaum et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

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Performance on a declarative memory task is better in high than low cortisol responders to psychosocial stress

Nater

Moor

Okere

et al. 2007

Psychoneuroendocrinology

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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Performance on a declarative memory task is better in high than low cortisol responders to psychosocial stress

Nater

Moor

Okere

et al. 2007

Psychoneuroendocrinology

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“…When pairing this evidence of cortisol reactivity in response to social identity threat with evidence that injections of cortisol directly impair cognitive functioning (Kirschbaum et al, 1996), it is clear that a physiological stress response could play a direct role in impairing task performance under stereotype threat (Path c in Figure 1). More research is needed to examine whether this specific hypothesis holds both in naturalistic situations of stereotype threat where the real-world implications of performance have greater power to produce a strong physiological stress response and in short-term laboratory contexts where the stakes are often lower.…”

Section: Cognitive Physiological and Affective Processes That Tax Wmentioning

confidence: 99%

An integrated process model of stereotype threat effects on performance.

Schmader

Johns

Forbes

2008

Psychological Review

1,293

1,175

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Research showing that activation of negative stereotypes can impair the performance of stigmatized individuals on a wide variety of tasks has proliferated. However, a complete understanding of the processes underlying these stereotype threat effects on behavior is still lacking. The authors examine stereotype threat in the context of research on stress arousal, vigilance, working memory, and selfregulation to develop a process model of how negative stereotypes impair performance on cognitive and social tasks that require controlled processing, as well as sensorimotor tasks that require automatic processing. The authors argue that stereotype threat disrupts performance via 3 distinct, yet interrelated, mechanisms: (a) a physiological stress response that directly impairs prefrontal processing, (b) a tendency to actively monitor performance, and (c) efforts to suppress negative thoughts and emotions in the service of self-regulation. These mechanisms combine to consume executive resources needed to perform well on cognitive and social tasks. The active monitoring mechanism disrupts performance on sensorimotor tasks directly. Empirical evidence for these assertions is reviewed, and implications for interventions designed to alleviate stereotype threat are discussed.

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“…Stress and the stress hormone corticosterone have profound impacts on both synaptic plasticity and memory, consistent with the role of memory in depression-associated behavioral changes. Stress or c orticosterone treatment enhances the acquisition of spatial information [61] , but also impairs the retrieval of memory [62] . Stress also enhances the acquisition of fear memory but impairs its extinction [63] .…”

mentioning

confidence: 99%

Rapid-onset antidepressant efficacy of glutamatergic system modulators: The neural plasticity hypothesis of depression

et al. 2014

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Depression is a devastating psychiatric disorder widely attributed to defi cient monoaminergic signaling in the central nervous system. However, most clinical antidepressants enhance monoaminergic neurotransmission with little delay but require 4−8 weeks to reach therapeutic efficacy, a paradox suggesting that the monoaminergic hypothesis of depression is an oversimplifi cation. In contrast to the antidepressants targeting the monoaminergic system, a single dose of the N-methyl-D-aspartate receptor (NMDAR) antagonist ketamine produces rapid (within 2 h) and sustained (over 7 days) antidepressant effi cacy in treatment-resistant patients. Glutamatergic transmission mediated by NMDARs is critical for experience-dependent synaptic plasticity and learning, processes that can be modifi ed indirectly by the monoaminergic system. To better understand the mechanisms of action of the new antidepressants like ketamine, we review and compare the monoaminergic and glutamatergic antidepressants, with emphasis on neural plasticity. The pathogenesis of depression may involve maladaptive neural plasticity in glutamatergic circuits that may serve as a new class of targets to produce rapid antidepressant effects.Keywords: depression; stress; neural plasticity; glutamatergic transmission; monoamine-based antidepressant; ketamine IntroductionDepression is a common psychiatric disorder, with prevalence rates of 19% in Beirut and 16.2% in the UnitedStates [1] . Depression is also one of the leading causes of severe mental disability, suicide, and socioeconomic burden, and its diagnosis sometimes relies on selfreported symptoms in the major depressive inventory [2,3] .The pathogenesis of depression is still not clear, and currently available antidepressants are far from satisfactory.Most antidepressants target the monoaminergic system [4] ; however, 30%-40% of patients are resistant to monoaminebased antidepressants (remittance rates of 13% to 36.8% with citalopram [5] ), and a clinically significant reduction of depressive symptoms in responders usually requires 4−8 weeks of daily treatment [6] . These limitations result in a large proportion of patients at high risk of suicide even after diagnosis. Thus, it is necessary to search for new antidepressants outside the monoaminergic system. R ecent clinical studies have demonstrated that a single dose of the N-methyl-D-aspartate receptor (NMDAR) antagonist ketamine has rapid antidepressant efficacy within 2 h that can be sustained for over 7 days in patients with treatment-resistant depression [7,8] . This finding suggests that depression could be directly associated with defi cits in glutamatergic synaptic transmission and plasticity. The monoaminergic hypothesis of depression, based on the efficacy of antidepressants that enhance monoaminergic transmission and signaling, has dominated the field of depression research for nearly half a century.However, the primacy of monoaminergic dysfunction in depression is inconsistent with the delay between enhancement of synaptic monoamines confer...

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Stress- and treatment-induced elevations of cortisol levels associated with impaired declarative memory in healthy adults

Cited by 727 publications

References 29 publications

Performance on a declarative memory task is better in high than low cortisol responders to psychosocial stress

Performance on a declarative memory task is better in high than low cortisol responders to psychosocial stress

An integrated process model of stereotype threat effects on performance.

Rapid-onset antidepressant efficacy of glutamatergic system modulators: The neural plasticity hypothesis of depression

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