Release of the hormone cortisol is normally tightly regulated. However, when regulation fails and cortisol is hypersecreted (as in Cushing’s disease), significant emotional changes occur, including depression, raising the question of whether cortisol effects on the brain could be generating depressive symptoms. Dysregulation leading to cortisol hypersecretion is also observed in depression, where emotion changes compose the core symptoms. However, cortisol as a causative agent in generating emotional changes in depression has rarely been investigated despite evidence that cortisol impacts emotional states and the neurophysiology of brain regions that process emotion. To explore the effects of cortisol on processes impacted by depression we administered exogenous cortisol to healthy subjects and observed its effects on the subjective experience of emotion, on brain activity patterns elicited by emotional stimuli, and on early perceptual processing of emotional stimuli. In a large neuroimaging study (N=60) we examined the effects of cortisol on brain activity induced by viewing emotionally evocative pictures (measured using fMRI) and on the cerebral hemodynamic response function, as a verification that cortisol’s physiological effects do not invalidate fMRI measures of brain activity. In this study we administered placebos to a control group and either a single dose regimen of cortisol administration (100mg) or an extended dose cortisol regimen (25mg/day, 5 days) (N=20/group) to experimental groups. In a separate behavioral study of early perceptual processing (N=33), we examined the effects of cortisol on detection and identification of emotional faces. Cortisol administration did not affect the cerebral hemodynamic response, but did significantly increased feelings of arousal during sadness and simultaneously inhibited subgenual cingulate (Brodmann area 25) activity, a region implicated in normal sadness and pathological sadness in depression. In the behavioral study, cortisol did not influence detection or identification of emotional faces. In summary, we demonstrate that cortisol, a hormone often hypersecreted in depression, influences the experience of emotions relevant to depression and activity in brain regions associated with depression, but it does not alter early perceptual processing of emotional stimuli. Further study of cortisol’s influence on these processes in healthy and depressed populations may provide insights into the pathophysiology of depression
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