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- Hypothalamus-Hypophysen-Nebennierenrinden-Achse (2) (entfernen)
Stress has been considered one of the most relevant factors promoting aggressive behavior. Animal and human pharmacological studies revealed the stress hormones corticosterone in rodents and cortisol in humans to constitute a particularly important neuroendocrine determinate in facilitating aggression and beyond that, assumedly in its continuation and escalation. Moreover, cortisol-induced alterations of social information processing, as well as of cognitive control processes, have been hypothesized as possible influencing factors in the stress-aggression link. So far, the immediate impact of a preceding stressor and thereby stress-induced rise of cortisol on aggressive behavior as well as higher-order cognitive control processes and social information processing in this context have gone mostly unheeded. The present thesis aimed to extend the hitherto findings of stress and aggression in this regard. For this purpose two psychophysiological studies with healthy adults were carried out, both using the socially evaluated-cold pressor test as an acute stress induction. Additionally to behavioral data and subjective reports, event related potentials were measured and acute levels of salivary cortisol were collected on the basis of which stressed participants were divided into cortisol-responders and "nonresponders. Study 1 examined the impact of acute stress-induced cortisol increase on inhibitory control and its neural correlates. 41 male participants were randomly assigned to the stress procedure or to a non-stressful control condition. Beforehand and afterwards, participants performed a Go Nogo task with visual letters to measure response inhibition. The effect of acute stress-induced cortisol increase on covert and overt aggressive behavior and on the processing of provoking stimuli within the aggressive encounter was investigated in study 2. Moreover, this experiment examined the combined impact of stress and aggression on ensuing affective information processing. 71 male and female participants were either exposed to the stress or to the control condition. Following this, half of each group received high or low levels of provocation during the Taylor Aggression Paradigm. At the end of the experiment, a passive viewing paradigm with affective pictures depicting positive, negative, or aggressive scenes with either humans or objects was realized. The results revealed that men were not affected by a stress-induced rise in cortisol on a behavioral level, showing neither impaired response inhibition nor enhanced aggressive behavior. In contrast, women showed enhanced overt and covert aggressive behavior under a surge of endogenous cortisol, confirming previous results, albeit only in case of high provocation and only up to the level of the control group. Unlike this rather moderate impact on behavior, cortisol showed a distinct impact on neural correlates of information processing throughout inhibitory control, aggression-eliciting stimuli, and emotional pictures for both men and women. At this, stress-induced increase of cortisol resulted in enhanced N2 amplitudes to Go stimuli, whereas P2 amplitudes to both and N2 to Nogo amplitudes retained unchanged, indicating an overcorrection and caution of the response activation in favor of successful inhibitory control. The processing of aggression-eliciting stimuli during the aggressive encounter was complexly altered by stress differently for women and men. Under increased cortisol levels, the frontal or parietal P3 amplitude patterns were either diminished or reversed in the case of high provocation compared to the control group and to cortisol-nonresponders, indicating a desensitization towards aggression-eliciting stimuli in males, but a more elaborate processing of those in women. Moreover, stress-induced cortisol and provocation jointly altered subsequent affective information processing at early as well as later stages of the information processing stream. Again, increased levels of cortisol led opposite directed amplitudes in the case of high provocation relative to the control group and cortisol-nonresponders, with enhanced N2 amplitudes in men and reduced P3 and LPP amplitudes in men and women for all affective pictures, suggesting initially enhanced emotional reactivity in men, but ensuing reduced motivational attention and enhanced emotion regulation in both, men and women. As a result, these present findings confirm the relevance of HPA activity in the elicitation and persistence of human aggressive behavior. Moreover, they reveal the significance of compensatory and emotion regulatory strategies and mechanisms in response to stress and provocation, indorsing the relevance of social information and cognitive control processes. Still, more research is needed to clarify the conditions which lead to the facilitation of aggression and by which compensatory mechanisms this is prevented.
Interaction between the Hypothalamic-Pituitary-Adrenal Axis and the Circadian Clock System in Humans
(2017)
Rotation of the Earth creates day and night cycles of 24 h. The endogenous circadian clocks sense these light/dark rhythms and the master pacemaker situated in the suprachiasmatic nucleus of the hypothalamus entrains the physical activities according to this information. The circadian machinery is built from the transcriptional/translational feedback loops generating the oscillations in all nucleated cells of the body. In addition, unexpected environmental changes, called stressors, also challenge living systems. A response to these stimuli is provided immediately via the autonomic-nervous system and slowly via the hypothalamus"pituitary"adrenal (HPA) axis. When the HPA axis is activated, circulating glucocorticoids are elevated and regulate organ activities in order to maintain survival of the organism. Both the clock and the stress systems are essential for continuity and interact with each other to keep internal homeostasis. The physiological interactions between the HPA axis and the circadian clock system are mainly addressed in animal studies, which focus on the effects of stress and circadian disturbances on cardiovascular, psychiatric and metabolic disorders. Although these studies give opportunity to test in whole body, apply unwelcome techniques, control and manipulate the parameters at the high level, generalization of the results to humans is still a debate. On the other hand, studies established with cell lines cannot really reflect the conditions occurring in a living organism. Thus, human studies are absolutely necessary to investigate mechanisms involved in stress and circadian responses. The studies presented in this thesis were intended to determine the effects of cortisol as an end-product of the HPA axis on PERIOD (PER1, PER2 and PER3) transcripts as circadian clock genes in healthy humans. The expression levels of PERIOD genes were measured under baseline conditions and after stress in whole blood. The results demonstrated here have given better understanding of transcriptional programming regulated by pulsatile cortisol at standard conditions and short-term effects of cortisol increase on circadian clocks after acute stress. These findings also draw attention to inter-individual variations in stress response as well as non-circadian functions of PERIOD genes in the periphery, which need to be examined in details in the future.