关键词: acute stress cognitive flexibility creativity eye blink rate eye movements pupillometry

Mesh : Humans Hydrocortisone Creativity Mental Processes / physiology Dopamine Blinking

来  源:   DOI:10.1111/psyp.14472

Abstract:
With the ever-changing social environment, individual creativity is facing a severe challenge induced by stress. However, little is known regarding the underlying mechanisms by which acute stress affects creative cognitive processing. The current research explored the impacts of the neuroendocrine response on creativity under stress and its underlying cognitive flexibility mechanisms. The enzyme-linked immuno sorbent assay was employed to assess salivary cortisol, which acted as a marker of stress-induced activation of the hypothalamic-pituitary-adrenal (HPA) axis. Eye blink rate (EBR) and pupil diameter were measured as respective indicators of dopamine and noradrenaline released by the activation of the sympathetic-adrenal-medullary (SAM) axis. The Wisconsin card task (WCST) measured cognitive flexibility, while the alternative uses task (AUT) and the remote association task (RAT) measured separately divergent and convergent thinking in creativity. Results showed higher cortisol increments following acute stress induction in the stress group than control group. Ocular results showed that the stress manipulation significantly increased EBR and pupil diameter compared to controls, reflecting increased SAM activity. Further analysis revealed that stress-released cortisol impaired the originality component of the AUT, reducing cognitive flexibility as measured by perseverative errors on the WCST task. Serial mediation analyses showed that both EBR and pupil diameter were also associated with increased perseverative errors leading to poor originality on the AUT. These findings confirm that physiological arousal under stress can impair divergent thinking through the regulation of different neuroendocrine pathways, in which the deterioration of flexible switching plays an important mediating role.
摘要:
随着社会环境的不断变化,个体创造力正面临着压力引发的严峻挑战。然而,关于急性压力影响创造性认知过程的潜在机制知之甚少。当前的研究探讨了神经内分泌反应对压力下创造力的影响及其潜在的认知灵活性机制。酶联免疫吸附试验用于评估唾液皮质醇,作为应激诱导的下丘脑-垂体-肾上腺(HPA)轴激活的标志。测量眨眼率(EBR)和瞳孔直径,分别作为交感神经-肾上腺-髓质(SAM)轴激活释放的多巴胺和去甲肾上腺素的指标。威斯康星卡任务(WCST)测量认知灵活性,而替代使用任务(AUT)和远程关联任务(RAT)分别测量创造力的发散和收敛思维。结果显示,应激组急性应激诱导后皮质醇增量高于对照组。眼部结果显示,与对照组相比,压力操作显着增加EBR和瞳孔直径,反映了SAM活动的增加。进一步的分析表明,释放压力的皮质醇损害了AUT的原创性成分,通过WCST任务上的持续错误来衡量,降低了认知灵活性。连续调解分析表明,EBR和瞳孔直径也与持续错误的增加有关,导致AUT的原创性较差。这些发现证实了压力下的生理唤醒可以通过调节不同的神经内分泌途径来削弱发散思维。其中柔性开关的恶化起着重要的中介作用。
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