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Many investigators have hypothesized that brain response to cortisol is altered in depression. However, neural activation in response to exogenously manipulated cortisol elevations has not yet been directly examined in depressed humans. Animal research shows that glucocorticoids have robust effects on hippocampal function, and can either enhance or suppress neuroplastic events in the hippocampus depending on a number of factors. We hypothesized that depressed individuals would show 1) altered hippocampal response to exogenous administration of cortisol, and 2) altered effects of cortisol on learning. In a repeated-measures design, 19 unmedicated depressed and 41 healthy individuals completed two fMRI scans. Fifteen mg oral hydrocortisone (i.e., cortisol) or placebo (order randomized and double-blind) was administered 1 h prior to encoding of emotional and neutral words during fMRI scans. Data analysis examined the effects of cortisol administration on 1) brain activation during encoding, and 2) subsequent free recall for words. Cortisol affected subsequent recall performance in depressed but not healthy individuals. We found alterations in hippocampal response to cortisol in depressed women, but not in depressed men (who showed altered response to cortisol in other regions, including subgenual prefrontal cortex). In both depressed men and women, cortisol's effects on hippocampal function were positively correlated with its effects on recall performance assessed days later. Our data provide evidence that in depressed compared to healthy women, cortisol's effects on hippocampal function are altered. Our data also show that in both depressed men and women, cortisol's effects on emotional memory formation and hippocampal function are related.
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Summary Stress disorders are among the most commonly occurring of all mental disorders. In this context, the question arises whether the stress inevitably unfolding around us has the potential to “contaminate” and compromise us. In the current multi-center study, we investigate the existence of such empathic stress (defined as a full-blown physiological stress response that arises solely by observing a target undergo a stressful situation), and whether empathic stress permeates to the core of the stress system, the hypothalamic-pituitary-adrenal (HPA) axis. Additionally, we investigate whether empathic stress responses may be modulated by the familiarity between observer and target (partners vs. strangers), the modality of observation (real-life vs. virtual) and observer sex (female vs. male). Participants were tested in dyads, paired with a loved one or a stranger of the opposite sex. While the target of the dyad (n = 151) was exposed to a psychosocial stressor, the observer (n = 211) watched through a one-way mirror or via live video transmission. Overall, 26% of the observers displayed physiologically significant cortisol increases. This empathic stress was more pronounced in intimate observer-target dyads (40%) and during the real-life representation of the stressor (30%). Empathic stress was further modulated by interindividual differences in empathy measures. Despite the higher prevalence of empathic stress in the partner and real-life observation conditions, significant cortisol responses also emerged in strangers (10%) and the virtual observation modality (24%). The occurrence of empathic stress down to the level of HPA-axis activation, in some cases even in total strangers and when only virtually witnessing another's distress, may have important implications for the development of stress-related diseases.
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The prefrontal cortex (PFC) has been well known for its role in higher order cognition, affect regulation and social reasoning. Although the precise underpinnings have not been sufficiently described, increasing evidence also supports a prefrontal involvement in the regulation of the hypothalamus-pituitary-adrenal (HPA) axis. Here we investigate the PFC's role in HPA axis regulation during a psychosocial stress exposure in 14 healthy humans. Regional brain metabolism was assessed using positron emission tomography (PET) and injection of fluoro-18-deoxyglucose (FDG). Depending on the exact location within the PFC, increased glucose metabolic rate was associated with lower or higher salivary cortisol concentration in response to a psychosocial stress condition. Metabolic glucose rate in the rostral medial PFC (mPFC) (Brodman area (BA) 9 and BA 10) was negatively associated with stress-induced salivary cortisol increases. Furthermore, metabolic glucose rate in these regions was inversely coupled with changes in glucose metabolic rate in other areas, known to be involved in HPA axis regulation such as the amygdala/hippocampal region. In contrast, metabolic glucose rate in areas more lateral to the mPFC was positively associated with saliva cortisol. Subjective ratings on task stressfulness, task controllability and self-reported dispositional mood states also showed positive and negative associations with the glucose metabolic rate in prefrontal regions. These findings suggest that in humans, the PFC is activated in response to psychosocial stress and distinct prefrontal metabolic glucose patterns are linked to endocrine stress measures as well as subjective ratings on task stressfulness, controllability as well as dispositional mood states.
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