Childhood maltreatment is extremely common in patients diagnosed with psychotic disorders. Moreover, it has been linked with impaired functioning of the Hypothalamic-Pituitary-Adrenal axis. Furthermore, abnormality of the HPA has been found in psychotic patients. Presence of childhood maltreatment could then explain why the HPA axis is dysfunctional in these subjects. Our objective was to clarify the role of childhood trauma in the cortisol profiles of psychotic patients. Thirty-one patients underwent assessments of childhood maltreatment. Diurnal cortisol and cortisol after a controlled psychosocial stress were also collected. Our results show that childhood trauma is associated with lower cortisol levels during the morning and during 24 hours. In men diagnosed with psychosis, childhood trauma is also associated with a higher cortisol response during psychosocial stress. This suggests an alteration of the HPA axis in psychotic patients, resulting from early trauma. Moreover, our results suggest that looking at specific types of childhood abuse may also be important.

In 1968, a study demonstrated that consolidated memories can be affected again if they are reactivated. Given the importance of the stress hormones glucocorticoids (GCs) on memory consolidation, the goal of the current study was to assess whether GCs had the capacity to affect a reactivated long-term memory and whether neutral and emotional memories were affected differently. At the first session, participants encoded a movie containing neutral and emotional scenes. Two days later, they recalled the story. Half of them were then exposed to a psychosocial stressor. Memory performance was assessed again right after the stressor and five days later. The stressed group recalled less neutral material five days after the stressor compared to controls. Immediately after the stressor, the stressed group recalled more emotional material than controls. Moreover, this enhanced memory trace was maintained across time. This highlights the importance of minimizing exposure to stressful contexts when reactivating emotional memories.

This Master's dissertation explored whether a rapid orienting of attention toward or away from social stress information during a restful state, relates to the magnitude of glucocorticoids (GC) released in response to a stressor, the Trier Social Stress Test (TSST). It also assessed whether childhood rearing in a low socioeconomic status (SES) context mediates this relationship. Subjects rested for 45 minutes during which time they completed a modified version of Posner's attention paradigm, comprising social stress words. Immediately following, participants were exposed to the stressor. Results indicated that a rapid attentional engagement toward social stress words associated with pronounced GC responses to the TSST. Fast engagers displayed lower self-esteem and did not differ in terms of their past SES. These findings demonstrate that attentional biases for social stress information at rest combine with diminished self-esteem to predict the magnitude of GC released during psychological stress irrespective of early SES conditions.

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The Hypothalamic Pituitary Adrenal (HPA) axis is the coordinator of adaptive responses to physical and psychological stress. The central nervous system plays a key role in modulation of both basal and adaptive HPA axis functions. In fact, since long ago, animal studies have shown that acute and chronic exposure to glucocorticoids (a stress hormone released due to HPA axis activation, cortisol in humans) affects the function and the morphology of brain areas such as the hippocampus and the cingulate cortex. This thesis is based on novel neuroimaging methodologies used to investigate the interactions of psychological stress, cortisol and the brain. It consists of three functional studies and a morphometric one. In the first functional study we show that the hippocampus (where glucocorticoid receptors are most abundant) plays a role in initiation of an HPA axis stress response. In the second study, we provide evidence that besides hippocampus, the neural activity in the so-called "default mode network" (DMN), especially the anterior cingulate cortex (ACC), relates to interindividual variations in HPA axis response to psychological stress. In the third study we have investigated the cortisol-modulation of the DMN. Again, we provide evidence for a role of the ACC and the orbitofrontal cortex in negative feedback inhibition of the HPA axis activity. Finally, we show a morphological link between the ACC and the cortisol response to awakening which is an index of basal HPA axis activity. Overall, our findings confirm the critical role of the ACC and mesolimbic system in HPA axis regulation. These findings also draw attention to the interactions between functional subregions of the medial prefrontal cortex and states of HPA axis function prior to stress onset---suggesting an interplay of the monitoring and the executive planning roles of the medial prefrontal cortex in behavioral adaptation to stress. Beyond stress research, our findings offer a framework for combining neuroimaging and neuroendocrinology to better understand the interindividual variances in behavior, and perhaps to better identify subgroups at risk of psychological disorders.

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