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Document Type

Poster

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Publication Date

4-2021

Keywords

stress, cognitive function

Abstract

In a variety of ways, stress affects memory, working quickly through catecholamines and more slowly through glucocorticoids. Catecholamine activities include beta adrenergic receptors and also glucose supply, while glucocorticoids modulate synaptic plasticity biphasically over hours and also create long-term improvements that last for weeks in the dendritic framework. By activating the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR), adrenal corticosterone, the primary stress hormone, will cause long-lasting effects on cognitive and emotional processes. Mounting research indicates that for certain psychiatric disorders, inadequate stress responses serve as a cause. Depression, for example, is synonymous with hypercortisolaemia (excessive cortisol, whereas hypocortisolaemia (insufficient cortisol) has been related to posttraumatic stress disorder (PTSD), arising from increased negative cortisol input. The prefrontal cortex, an area regulating high-level "executive" tasks, including working memory, distraction avoidance, novelty finding, and decision making, is one of the main targets of stress hormones. In adult animals, recurrent stress or glucocorticoid therapy has been shown to induce systemic remodeling and behavioural modifications in the prefrontal cortex, such as dendritic shortening, spine loss and cortical atrophy, as well as deficiency in cognitive flexibility and perceptual focus. As pathways influencing the detrimental impacts of stress on cognition, both subjective anxiety and cognitive interference were suggested. Aging tests have found that anxiety is correlated with poorer cognitive efficiency, but according to studies, implications of cognitive interference have not been studied by anyone.

First Advisor

Becky Wolff

Research Area

Health Sciences

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