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Inflexibly focused under stress: acute psychosocial stress increases shielding of action goals at the expense of reduced cognitive flexibility with increasing time lag to the stressor.
J Cogn Neurosci. 2011 Nov; 23(11):3218-27.JC

Abstract

Dynamically adjusting the right amount of goal shielding to varying situational demands is associated with the flexibility of cognitive control, typically linked with pFC functioning. Although stress hormones are found to also bind to prefrontal receptors, the link between stress and cognitive control remains elusive. Based on that, we aimed at investigating effects of acute psychosocial stress on dynamic control adjustments. Forty-eight healthy volunteers were exposed to either a well-established stress induction protocol (the Trier Social Stress Test, TSST) or a standardized control situation before a selective attention (Simon) task involving response conflicts. The individual physiological stress response was monitored by analyzing levels of free cortisol and α-amylase activity in saliva samples showing that the TSST reliably induced an increase of endogenous stress hormone levels. Acute stress did not inevitably impair cognitive functioning, however, as stressed participants showed tonically increased goal shielding (to reduce interference) at the expense of decreased cognitive flexibility. Importantly, as a novel finding in humans, stress effects on cognitive functions were not present immediately after the stress experience but developed gradually over time and, therefore, paralleled the time course of the hypothalamus-pituitary-adrenal (HPA) stress response. In addition, the total increase of individual cortisol levels reflecting HPA activity, but not the total changes in α-amylase activity associated with sympathetic activity, was reversely related to the amount of cognitive flexibility in the final block of testing. Our study provides evidence for a stress-induced time-dependent decrease of cognitive flexibility that might be related to changes in cortisol levels.

Authors+Show Affiliations

Technische Universität Dresden, Dresden, Germany. plessow@biopsych.tu-dresden.deNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

21452940

Citation

Plessow, Franziska, et al. "Inflexibly Focused Under Stress: Acute Psychosocial Stress Increases Shielding of Action Goals at the Expense of Reduced Cognitive Flexibility With Increasing Time Lag to the Stressor." Journal of Cognitive Neuroscience, vol. 23, no. 11, 2011, pp. 3218-27.
Plessow F, Fischer R, Kirschbaum C, et al. Inflexibly focused under stress: acute psychosocial stress increases shielding of action goals at the expense of reduced cognitive flexibility with increasing time lag to the stressor. J Cogn Neurosci. 2011;23(11):3218-27.
Plessow, F., Fischer, R., Kirschbaum, C., & Goschke, T. (2011). Inflexibly focused under stress: acute psychosocial stress increases shielding of action goals at the expense of reduced cognitive flexibility with increasing time lag to the stressor. Journal of Cognitive Neuroscience, 23(11), 3218-27. https://doi.org/10.1162/jocn_a_00024
Plessow F, et al. Inflexibly Focused Under Stress: Acute Psychosocial Stress Increases Shielding of Action Goals at the Expense of Reduced Cognitive Flexibility With Increasing Time Lag to the Stressor. J Cogn Neurosci. 2011;23(11):3218-27. PubMed PMID: 21452940.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inflexibly focused under stress: acute psychosocial stress increases shielding of action goals at the expense of reduced cognitive flexibility with increasing time lag to the stressor. AU - Plessow,Franziska, AU - Fischer,Rico, AU - Kirschbaum,Clemens, AU - Goschke,Thomas, Y1 - 2011/03/31/ PY - 2011/4/2/entrez PY - 2011/4/2/pubmed PY - 2012/2/9/medline SP - 3218 EP - 27 JF - Journal of cognitive neuroscience JO - J Cogn Neurosci VL - 23 IS - 11 N2 - Dynamically adjusting the right amount of goal shielding to varying situational demands is associated with the flexibility of cognitive control, typically linked with pFC functioning. Although stress hormones are found to also bind to prefrontal receptors, the link between stress and cognitive control remains elusive. Based on that, we aimed at investigating effects of acute psychosocial stress on dynamic control adjustments. Forty-eight healthy volunteers were exposed to either a well-established stress induction protocol (the Trier Social Stress Test, TSST) or a standardized control situation before a selective attention (Simon) task involving response conflicts. The individual physiological stress response was monitored by analyzing levels of free cortisol and α-amylase activity in saliva samples showing that the TSST reliably induced an increase of endogenous stress hormone levels. Acute stress did not inevitably impair cognitive functioning, however, as stressed participants showed tonically increased goal shielding (to reduce interference) at the expense of decreased cognitive flexibility. Importantly, as a novel finding in humans, stress effects on cognitive functions were not present immediately after the stress experience but developed gradually over time and, therefore, paralleled the time course of the hypothalamus-pituitary-adrenal (HPA) stress response. In addition, the total increase of individual cortisol levels reflecting HPA activity, but not the total changes in α-amylase activity associated with sympathetic activity, was reversely related to the amount of cognitive flexibility in the final block of testing. Our study provides evidence for a stress-induced time-dependent decrease of cognitive flexibility that might be related to changes in cortisol levels. SN - 1530-8898 UR - https://www.unboundmedicine.com/medline/citation/21452940/Inflexibly_focused_under_stress:_acute_psychosocial_stress_increases_shielding_of_action_goals_at_the_expense_of_reduced_cognitive_flexibility_with_increasing_time_lag_to_the_stressor_ L2 - https://www.mitpressjournals.org/doi/10.1162/jocn_a_00024?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -