Cortisol is a glucocorticoid hormone secreted by the adrenal cortex that serves as the primary mediator of the stress response. During acute stress, it elevates blood glucose and temporarily enhances attention and arousal as an adaptive survival mechanism. However, chronic elevation suppresses hippocampal neurogenesis and reduces synaptic plasticity in the prefrontal cortex, impairing memory and executive function.
Cortisol Secretion Mechanisms
Cortisol is released through the hypothalamic-pituitary-adrenal (HPA) axis. When the hypothalamus detects stress, it releases corticotropin-releasing hormone (CRH), which triggers ACTH secretion from the anterior pituitary, ultimately stimulating cortisol release from the adrenal cortex. Secretion follows a circadian rhythm, peaking shortly after waking (the cortisol awakening response) and reaching its lowest point at night.
Acute Stress and Cognitive Performance
Brief cortisol elevation raises blood glucose and temporarily enhances attention and arousal. However, one review reports that even mild acute uncontrollable stress can rapidly impair the higher-order cognitive abilities supported by the prefrontal cortex.
Chronic Stress and Long-term Cognitive Impact
Repeated stress causes dendritic atrophy in the hippocampal CA3 region and suppresses neurogenesis in the dentate gyrus. Besides glucocorticoids, excitatory amino acids and NMDA receptors are involved in these two changes. More prolonged stress also produces structural changes in prefrontal dendrites.