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Human memory under stress: The glucocorticoid-glutamate mediation hypothesis

Subject Area Biological Psychology and Cognitive Neuroscience
Term since 2021
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 461443071
 
The present project aims at investigating how acute stress can simultaneously improve certain memory processes in humans but worsen others. To explain such diametral stress effect patterns in rodents, the glucocorticoid-glutamate mediation hypothesis was developed. It assumes that acute stress affects cognitive-behavioral processes by modulatory actions of glucocorticoidal stress hormones on the glutamate N-methyl-D-aspartate receptor (NMDAR). Since acute stress and glucocorticoidal stress hormones appear to increase glutamate turnover at NMDARs in some brain regions but decrease it in others, the same glucocorticoid-induced mechanism might explain both higher and lower memory performances under stress. To evaluate the predictive value of the glucocorticoid-glutamate mediation hypothesis towards human memory under acute stress, two interventional psychopharmacological stress studies are proposed. In addition to the assessment of various NMDAR-associated and putatively stress- and glucocorticoid-sensitive memory processes (i.e., ultra-short-term, short-term, working and long-term memory capacities), these studies rely on the combination of a standardized stress-induction protocol with pharmacological manipulations of the presumed stress effect mediators (i.e., the availability of the glucocorticoidal stress hormone cortisol and/or NMDARs). By manipulating both the exposition factor (stress or cortisol availability) and the potential mediator of its effects on human memory processes (NMDAR availability), this project aims to empirically investigate the (mediation) effects of acute stress and the glucocorticoidal stress hormone cortisol as well as the presumed causal mediation mechanism of acute stress on human memory processes.
DFG Programme Research Grants
 
 

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