STRESS, CORTISOL, AND COGNITIVE FUNCTION

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The specific aims of this project are to: (1) Dissociate immediate and delayed effects of acutely elevated cortisol levels on cognitive function; and (2) Establish the relationship between the magnitude of acute increases in cortisol secretion and changes in long-term memory. Cortisol is a steroid hormone released from the adrenal glands in response to physical or psychological stress. A number of studies have reported cognitive changes in humans associated with acute and chronic elevations in cortisol, including deficits in attention and verbal memory. It is reasonable to presume that these cognitive changes are the result of cortisol's actions on neural tissue. We know that cortisol's effects on neural tissue are complex and nonlinear, depending on amount and timing. What we do not yet understand is how cortisol's complex interactions with neural tissue affect cognitive function. This experiment tests the proposal that stress-induced increases in cortisol will have differing effects on cognition depending on two interacting factors: (a) the duration of increase in cortisol secretion, and (b) the magnitude of increase in cortisol secretion. The immediate effects of increased cortisol may be to enhance immediate and short-term cognitive processes, (e.g. attention and memory encoding), while the delayed effects may be to interfere with long-term processes (e.g. memory consolidation and storage). At the same time, however, moderate increases in cortisol may enhance long-term processes, while relatively large increases may have detrimental effects. This experiment is designed to dissociate the duration and magnitude effects of cortisol on attention and memory. It tests three specific hypotheses: (a) Immediate attentional processes and short-term memory will be enhanced when acute elevations in cortisol are induced in the laboratory; (b) Moderate acute increases in cortisol will be associated with long-term memory enhancements ; and (c) Relatively large acute elevations in cortisol will be associated with long-term memory impairments. The hypotheses will be tested by inducing stress in a group of human participants and measuring (a) self-report, physiological, and cortisol indicators of stress, and (b) performance on attention and memory tasks. These pilot studies will provide the foundation for exploring chronic, hippocampus-mediated memory disorders associated with chronic stress and elevated cortisol.