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- Elektroencephalogramm (3) (entfernen)
Phase-amplitude cross-frequency coupling is a mechanism thought to facilitate communication between neuronal ensembles. The mechanism could underlie the implementation of complex cognitive processes, like executive functions, in the brain. This thesis contributes to answering the question, whether phase-amplitude cross-frequency coupling - assessed via electroencephalography (EEG) - is a mechanism by which executive functioning is implemented in the brain and whether an assumed performance effect of stress on executive functioning is reflected in phase-amplitude coupling strength. A huge body of studies shows that stress can influence executive functioning, in essence having detrimental effects. In two independent studies, each being comprised of two core executive function tasks (flexibility and behavioural inhibition as well as cognitive inhibition and working memory), beta-gamma phase-amplitude coupling was robustly detected in the left and right prefrontal hemispheres. No systematic pattern of coupling strength modulation by either task demands or acute stress was detected. Beta-gamma coupling might also be present in more basic attention processes. This is the first investigation of the relationship between stress, executive functions and phase-amplitude coupling. Therefore, many aspects have not been explored yet. For example, studying phase precision instead of coupling strength as an indicator for phase-amplitude coupling modulations. Furthermore, data was analysed in source space (independent component analysis); comparability to sensor space has still to be determined. These as well as other aspects should be investigated, due to the promising finding of very robust and strong beta-gamma coupling for all executive functions. Additionally, this thesis tested the performance of two widely used phase-amplitude coupling measures (mean vector length and modulation index). Both measures are specific and sensitive to coupling strength and coupling width. The simulation study also drew attention to several confounding factors, which influence phase-amplitude coupling measures (e. g. data length, multimodality).
Aggression is one of the most researched topics in psychology. This is understandable, since aggression behavior does a lot of harm to individuals and groups. A lot is known already about the biology of aggression, but one system that seems to be of vital importance in animals has largely been overlooked: the hypothalamic-pituitary-adrenal (HPA) axis. Menno Kruk and Jószef Haller and their research teams developed rodent models of adaptive, normal, and abnormal aggressive behavior. They found the acute HPA axis (re)activity, but also chronic basal levels to be causally relevant in the elicitation and escalation of aggressive behavior. As a mediating variable, changes in the processing of relevant social information is proposed, although this could not be tested in animals. In humans, not a lot of research has been done, but there is evidence for both the association between acute and basal cortisol levels in (abnormal) aggression. However, not many of these studies have been experimental of nature. rnrnOur aim was to add to the understanding of both basal chronic levels of HPA axis activity, as well as acute levels in the formation of aggressive behavior. Therefore, we did two experiments, both with healthy student samples. In both studies we induced aggression with a well validated paradigm from social psychology: the Taylor Aggression Paradigm. Half of the subjects, however, only went through a non-provoking control condition. We measured trait basal levels of HPA axis activity on three days prior. We took several cortisol samples before, during, and after the task. After the induction of aggression, we measured the behavioral and electrophysiological brain response to relevant social stimuli, i.e., emotional facial expressions embedded in an emotional Stroop task. In the second study, we pharmacologically manipulated cortisol levels 60min before the beginning of the experiment. To do that, half of the subjects were administered 20mg of hydrocortisone, which elevates circulating cortisol levels (cortisol group), the other half was administered a placebo (placebo group). Results showed that acute HPA axis activity is indeed relevant for aggressive behavior. We found in Study 1 a difference in cortisol levels after the aggression induction in the provoked group compared to the non-provoked group (i.e., a heightened reactivity of the HPA axis). However, this could not be replicated in Study 2. Furthermore, the pharmacological elevation of cortisol levels led to an increase in aggressive behavior in women compared to the placebo group. There were no effects in men, so that while men were significantly more aggressive than women in the placebo group, they were equally aggressive in the cortisol group. Furthermore, there was an interaction of cortisol treatment with block of the Taylor Aggression Paradigm, in that the cortisol group was significantly more aggressive in the third block of the task. Concerning basal HPA axis activity, we found an effect on aggressive behavior in both studies, albeit more consistently in women and in the provoked and non-provoked groups. However, the effect was not apparent in the cortisol group. After the aggressive encounter, information processing patterns were changed in the provoked compared to the non-provoked group for all facial expressions, especially anger. These results indicate that the HPA axis plays an important role in the formation of aggressive behavior in humans, as well. Importantly, different changes within the system, be it basal or acute, are associated with the same outcome in this task. More studies are needed, however, to better understand the role that each plays in different kinds of aggressive behavior, and the role information processing plays as a possible mediating variable. This extensive knowledge is necessary for better behavioral interventions.
In der vorliegenden Dissertation wurde Belohnungssensitivität mit Spielverhalten und elektrophysiologischen Korrelaten wie dem Ruhe-EEG und ereigniskorrelierten Potenzialen auf Feedback-Reize in Verbindung gebracht. Belohnungssensitivität ist nach der zugrundeliegenden Definition als Konstrukt mit mehreren Facetten zu verstehen, die eng mit Extraversion, positiver Affektivität, dem Behavioral Activation System, Novelty Seeking, Belohnungsabhängigkeit und Selbstwirksamkeit assoziiert sind. Bei der Untersuchung einer spezifischen Spielsituation, in der 48 gesunde Studentinnen durch eigene Entscheidungen Belohnungen erhalten konnten, zeigte sich, dass das Spielverhalten mit den während des Spiels erfassten ereigniskorrelierten Potentialen (hier: FRN (feedback related negativity)und P300) auf die Belohnungssignale in Form eines Feedbacks korreliert. Belohnungssensitive Personen zeigen tendenziell nach einem Gewinn-Feedback eine weniger negative FRN-Amplitude, die wiederum positiv mit der gewählten Einsatzhöhe assoziiert ist. Auch die Amplitude der P300 scheint mit dem Spielverhalten zusammenzuhängen. So zeigte sich ein positiver Zusammenhang zwischen typisch belohnungssensitivem Verhalten und der mittleren Amplitude der P300: Gewinne gehen mit einer größeren P300-Positivierung und schnelleren Entscheidungen im Spiel einher. Dagegen konnte weder das Spielverhalten noch die über diverse Fragebögen erfasste Ausprägung der Belohnungssensitivität in der kortikalen Grundaktivierung im Ruhezustand einer Person abgebildet werden. Die vorliegenden Ergebnisse deuten darauf hin, dass Belohnungssensitivität ein Persönlichkeitsmerkmal ist, das sich sowohl im Verhalten, als auch in der elektrokortikalen Aktivität in belohnungsrelevanten Situationen widerspiegelt.