Hydrocortisone accelerates the decay of iconic memory traces: on the modulation of executive and stimulus-driven constituents of sensory information maintenance.

Autor: Miller R; Department of Psychology, Technische Universität Dresden, Dresden, Germany. Electronic address: robert.miller@tu-dresden.de., Weckesser LJ; Department of Psychology, Technische Universität Dresden, Dresden, Germany., Smolka MN; Department of Psychiatry and Neuroimaging Center, Technische Universität Dresden, Dresden, Germany., Kirschbaum C; Department of Psychology, Technische Universität Dresden, Dresden, Germany., Plessow F; Department of Psychology, Technische Universität Dresden, Dresden, Germany; Berenson-Allen Center for Noninvasive Brain Stimulation, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Jazyk: angličtina
Zdroj: Psychoneuroendocrinology [Psychoneuroendocrinology] 2015 Mar; Vol. 53, pp. 148-58. Date of Electronic Publication: 2015 Jan 03.
DOI: 10.1016/j.psyneuen.2014.12.016
Abstrakt: A substantial amount of research documents the impact of glucocorticoids on higher-order cognitive functioning. By contrast, surprisingly little is known about the susceptibility of basic sensory processes to glucocorticoid exposure given that the glucocorticoid receptor density in the human visual cortex exceeds those observed in prefrontal and most hippocampal brain regions. As executive tasks also rely on these sensory processes, the present study investigates the impact of glucocorticoid exposure on different performance parameters characterizing the maintenance and transfer of sensory information from iconic memory (IM; the sensory buffer of the visual system) to working memory (WM). Using a crossover factorial design, we administered one out of three doses of hydrocortisone (0.06, 0.12, or 0.24mg/kg bodyweight) and a placebo to 18 healthy young men. Thereafter participants performed a partial report task, which was used to assess their individual ability to process sensory information. Blood samples were concurrently drawn to determine free and total cortisol concentrations. The compiled pharmacokinetic and psychophysical data demonstrates that free cortisol specifically accelerated the decay of sensory information (r=0.46) without significantly affecting the selective information transfer from IM to WM or the capacity limit of WM. Specifically, nonparametric regression revealed a sigmoid dose-response relationship between free cortisol levels during the testing period and the IM decay rates. Our findings highlight that glucocorticoid exposure may not only impact on the recruitment of top-down control for an active maintenance of sensory information, but alter their passive (stimulus-driven) maintenance thereby changing the availability of information prior to subsequent executive processing.
(Copyright © 2014 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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