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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.
Stress represents a significant problem for Western societies inducing costs as high as 3-4 % of the European gross national products, a burden that is continually increasing (WHO Briefing, EUR/04/5047810/B6). The classical stress response system is the hypothalamic-pituitary-adrenal (HPA) axis which acts to restore homeostasis after disturbances. Two major components within the HPA axis system are the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR). Cortisol, released from the adrenal glands at the end of the HPA axis, binds to MRs and with a 10 fold lower affinity to GRs. Both, impairment of the HPA axis and an imbalance in the MR/GR ratio enhances the risk for infection, inflammation and stress related psychiatric disorders. Major depressive disorder (MDD) is characterised by a variety of symptoms, however, one of the most consistent findings is the hyperactivity of the HPA axis. This may be the result of lower numbers or reduced activity of GRs and MRs. The GR gene consists of multiple alternative first exons resulting in different GR mRNA transcripts whereas for the MR only two first exons are known to date. Both, the human GR promoter 1F and the homologue rat Gr promoter 1.7 seem to be susceptible to methylation during stressful early life events resulting in lower 1F/1.7 transcript levels. It was proposed that this is due to methylation of a NGFI-A binding site in both, the rat promoter 1.7 and the human promoter 1F. The research presented in this thesis was undertaken to determine the differential expression and methylation patterns of GR and MR variants in multiple areas of the limbic brain system in the healthy and depressed human brain. Furthermore, the transcriptional control of the GR transcript 1F was investigated as expression changes of this transcript were associated with MDD, childhood abuse and early life stress. The role of NGFI-A and several other transcription factors on 1F regulation was studied in vitro and the effect of Ngfi-a overexpression on the rat Gr promoter 1.7 in vivo. The susceptibility to epigenetic programming of several GR promoters was investigated in MDD. In addition, changes in methylation levels have been determined in response to a single acute stressor in rodents. Our results showed that GR and MR first exon transcripts are differentially expressed in the human brain, but this is not due to epigenetic programming. We showed that NGFI-A has no effect on endogenous 1F/1.7 expression in vitro and in vivo. We provide evidence that the transcription factor E2F1 is a major element in the transcriptional complex necessary to drive the expression of GR 1F transcripts. In rats, highly individual methylation patterns in the paraventricular nucleus of the hypothalamus (PVN) suggest that this is not related to the stressor but can rather be interpreted as pre-existing differences. In contrast, the hippocampus showed a much more uniform epigenetic status, but still is susceptible to epigenetic modification even after a single acute stress suggesting a differential "state‟ versus "trait‟ regulation of the GR gene in different brain regions. The results of this thesis have given further insight in the complex transcriptional regulation of GR and MR first exons in health and disease. Epigenetic programming of GR promoters seems to be involved in early life stress and acute stress in adult rats; however, the susceptibility to methylation in response to stress seems to vary between brain regions.
The catechol-O-methyltransferase gene (COMT) plays a crucial role in the metabolism of catecholamines in the frontal cortex. A single nucleotide polymorphism (Val158Met SNP, rs4680) leads to either methionine (Met) or valine (Val) at codon 158, resulting in a three- to fourfold reduction in COMT activity. The aim of the present study was to assess the COMT Val158Met SNP as a risk factor for attention-deficit/hyperactivity disorder (ADHD), ADHD symptom severity and co-morbid conduct disorder (CD) in 166 children with ADHD. The main finding of the present study is that the Met allele of the COMT Val158Met SNP was associated with ADHD and increased ADHD symptom severity. No association with co-morbid CD was observed. In addition, ADHD symptom severity and early adverse familial environment were positive predictors of lifetime CD. These findings support previous results implicating COMT in ADHD symptom severity and early adverse familial environment as risk factors for co-morbid CD, emphasizing the need for early intervention to prevent aggressive and maladaptive behavior progressing into CD, reducing the overall severity of the disease burden in children with ADHD.
The last decades of stress research have yielded substantial advancements highlighting the importance of the phenomenon for basic psychological functions as well as physical health and well-being. Progress in stress research heavily relies on the availability of suitable and well validated laboratory stressors. Appropriate laboratory stressors need to be able to reliably provoke a response in the relevant parameters and be applicable in different research settings or experimental designs. This thesis focuses on the Cold Pressor Test (CPT) as a stress induction technique. Three published experiments are presented that show how the advantages of the CPT can be used to test stress effects on memory processes and how some of its disadvantages can be met by a simple modification that retains its feasibility and validity. The first experiment applies the CPT in a substantial sample to investigate the consolidation effects of post-learning sympathetic arousal. Stressed participants with high increases in heart rate during the CPT showed enhanced memory performance one day after learning compared to both the warm water control group and low heart rate responders. This finding suggests that beta-adrenergic activation elicited shortly after learning enhances memory consolidation and that the CPT induced heart rate response is a predictor for this effect. Moreover, the CPT proved to be an appropriate stressor to test hypothesis about endogenous adrenergic effects on memory processes. The second experiment addresses known practical limitations of the standard dominant hand CPT protocol. A bilateral feet CPT modification is presented, the elicited neuroendocrine stress response assessed and validated against the standard CPT in a within-subjects design. The bilateral feet CPT elicited a substantial neuroendocrine stress response. Moreover, with the exception of blood pressure responses, all stress parameters were enhanced compared to the standard CPT. This shows that the bilateral feet CPT is a valid alternative to the standard CPT. The third experiment further validates the bilateral feet CPT and its corresponding control procedure by employing it in a typical application scenario. Specifically, the bilateral feet CPT was used to modulate retrieval of event files in a distractor-response binding paradigm that required lateralized bimanual responses. Again, the bilateral feet CPT induced significant increases in heart rate, blood pressure and cortisol, no such increases could be observed in the warm water control condition. Moreover, stressed participants showed diminished retrieval compared to controls. These results provide further evidence for the feasibility and validity of the bilateral feet CPT and its warm water control procedure. Together the experiments presented here highlight the usefulness of the CPT as a tool in psychophysiological stress research. It is especially well suited to test hypothesis concerning stress effects on memory processes and its applicability can be further increased by the bilateral feet modification.
Memory consists of multiple anatomically and functionally distinct systems. Animal studies suggest that stress modulates multiple memory systems in a manner that favors nucleus caudatus-based stimulus-response learning at the expense of hippocampus-based spatial learning. The present work aimed (i) to translate these findings to humans, (ii) to determine the involvement of the stress hormone cortisol in this effect, and (iii) to assess whether the use of stimulus-response and spatial strategies is a long lasting person characteristic. To address these issues we developed a new paradigm that differentiates the use of spatial and stimulus-response learning in humans. Our findings indicate that (i) psychosocial stress (Trier Social Stress Test) modulates the use of spatial and stimulus-response learning in humans, (ii) cortisol plays a key role in this modulatory effect of stress, and (iii) the use of spatial and stimulus-response learning is affected by situational rather than long lasting person factors.
Stress is a common phenomenon for animals living in the wild, but also for humans in modern societies. Originally, the body's stress response is an adaptive reaction to a possibly life-threatening situation, and it has been shown to impact on energy distribution and metabolism, thereby increasing the chance of survival. However, stress has also been shown to impact on mating behaviour and reproductive strategies in animals and humans. This work deals with the effect of stress on reproductive behavior. Up to now, research has only focused on the effects of stress on reproduction in general. The effects of stress on reproduction may be looked at from two points of view. First, stress affects reproductive functioning by endocrine (e.g. glucocorticoid) actions on the reproductive system. However, stress can also influence reproductive behavior, i.e. mate choice and mating preferences. Animals and humans do not mate randomly, but exhibit preferences towards mating partners. One factor by which animals and humans choose their mating partners is similarity vs. dissimilarity: Similar mates usually carry more of one's own genes and the cooperation between similar mates is, at least theoretically, less hampered by expressing diverse behaviors. By mating with dissimilar mates on the other hand one may acquire new qualities for oneself, but also for one's offspring, useful to cope with environmental challenge. In humans we usually find a preference for similar mates. Due to the high costs of breeding, variables like cooperation and life-long partnerships may play a greater role than the acquaintance of new qualities.The present work focuses on stress effects on mating preferences of humans and will give a first answer to the question whether stress may affect our preference for similar mates. Stress and mating preferences are at the centre of this work. Thus, in the first Chapter I will give an introduction on stress and mating preferences and link these topics to each other. Furthermore, I will give a short summary of the studies described in Chapter II - Chapter IV and close the chapter with a general discussion of the findings and directions for further research on stress and mating preferences. Human mating behavior is complex, and many aspects of it may not relate to biology but social conventions and education. This work will not focus on those aspects but rather on cognitive and affective processing of erotic and sexually-relevant stimuli, since we assume that these aspects of mating behaviour are likely related to psychobiological stress mechanisms. Therefore, a paradigm is needed that measures such aspects of mating preferences in humans. The studies presented in Chapter II and Chapter III were performed in order to develop such a paradigm. In these studies we show that affective startle modulation may be used to indicate differences in sexual approach motivation to potential mating partners with different similarity levels to the participant. In Chapter IV, I will describe a study that aimed to investigate the effects of stress on human mating preferences. We showed that stress reverses human mating preferences: While unstressed individuals show a preference for similar mates, stressed individuals seem to prefer dissimilar mates. Overall, the studies presented in this work showed that affective startle modulation can be employed to measure mating preferences in humans and that these mating preferences are influenced by stress.
The brain is the central coordinator of the human stress reaction. At the same time, peripheral endocrine and neural stress signals act on the brain modulating brain function. Here, three experimental studies are presented demonstrating this dual role of the brain in stress. Study I shows that centrally acting insulin, an important regulator of energy homeostasis, attenuates the stress related cortisol secretion. Studies II and III show that specific components of the stress reaction modulate learning and memory retrieval, two important aspects of higher-order brain function.
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.
Fostering positive and realistic self-concepts of individuals is a major goal in education worldwide (Trautwein & Möller, 2016). Individuals spend most of their childhood and adolescence in school. Thus, schools are important contexts for individuals to develop positive self-perceptions such as self-concepts. In order to enhance positive self-concepts in educational settings and in general, it is indispensable to have a comprehensive knowledge about the development and structure of self-concepts and their determinants. To date, extensive empirical and theoretical work on antecedents and change processes of self-concept has been conducted. However, several research gaps still exist, and several of these are the focus of the present dissertation. Specifically, these research gaps encompass (a) the development of multiple self-concepts from multiple perspectives regarding stability and change, (b) the direction of longitudinal interplay between self-concept facets over the entire time period from childhood to late adolescence, and (c) the evidence that a recently developed structural model of academic self-concept (nested Marsh/Shavelson model [Brunner et al., 2010]) fits the data in elementary school students, (d) the investigation of structural changes in academic self-concept profile formation within this model, (e) the investigation of dimensional comparison processes as determinants of academic self-concept profile formation in elementary school students within the internal/external frame of reference model (I/E model; Marsh, 1986), (f) the test of moderating variables for dimensional comparison processes in elementary school, (g) the test of the key assumptions of the I/E model that effects of dimensional comparisons depend to a large degree on the existence of achievement differences between subjects, and (h) the generalizability of the findings regarding the I/E model over different statistical analytic methods. Thus, the aim of the present dissertation is to contribute to close these gaps with three studies. Thereby, data from German students enrolled in elementary school to secondary school education were gathered in three projects comprising the developmental time span from childhood to adolescence (ages 6 to 20). Three vital self-concept areas in childhood and adolescence were in-vestigated: general self-concept (i.e., self-esteem), academic self-concepts (general, math, reading, writing, native language), and social self-concepts (of acceptance and assertion). In all studies, data were analyzed within a latent variable framework. Findings are discussed with respect to the research aims of acquiring more comprehensive knowledge on the structure and development of significant self-concept in childhood and adolescence and their determinants. In addition, theoretical and practical implications derived from the findings of the present studies are outlined. Strengths and limitations of the present dissertation are discussed. Finally, an outlook for future research on self-concepts is given.
Every day we are exposed to a large set of appetitive food cues, mostly of high caloric, high carbohydrate content. Environmental factors like food cue exposition can impact eating behavior, by triggering anticipatory endocrinal responses and reinforcing the reward value of food. Additionally, it has been shown that eating behavior is largely influence by neuroendocrine factors. Energy homeostasis is of great importance for survival in all animal species. It is challenged under the state of food deprivation which is considered to be a metabolic stressor. Interestingly, the systems regulating stress and food intake share neural circuits. Adrenal glucocorticoids, as cortisol, and the pancreatic hormone insulin have been shown to be crucial to maintain catabolic and anabolic balance. Cortisol and insulin can cross the blood-brain barrier and interact with receptors distributed throughout the brain, influencing appetite and eating behavior. At the same time, these hormones have an important impact on the stress response. The aim of the current work is to broaden the knowledge on reward related food cue processing. With that purpose, we studied how food cue processing is influenced by food deprivation in women (in different phases of the menstrual cycle) and men. Furthermore, we investigated the impact of the stress/metabolic hormones, insulin and cortisol, at neural sites important for energy metabolism and in the processing of visual food cues. The Chapter I of this thesis details the underlying mechanisms of the startle response and its application in the investigation of food cue processing. Moreover, it describes the effects of food deprivation and of the stress-metabolic hormones insulin and cortisol in reward related processing of food cues. It explains the rationale for the studies presented in Chapter II-IV and describes their main findings. A general discussion of the results and recommendations for future research is given. In the study described in Chapter II, startle methodology was used to study the impact of food deprivation in the processing of reward related food cues. Women in different phases of the menstrual cycle and men were studied, in order to address potential effects of sex and menstrual cycle. All participants were studied either satiated or food deprived. Food deprivation provoked enhanced acoustic startle (ASR) response during foreground presentation of visual food cues. Sex and menstrual cycle did not influence this effect. The startle pattern towards food cues during fasting can be explained by a frustrative nonreward effect (FNR), driven by the impossibility to consume the exposed food. In Chapter III, a study is described, which was carried out to explore the central effects of insulin and cortisol, using continuous arterial spin labeling to map cerebral blood flow patterns. Following standardized periods of fasting, male participants received either intranasal insulin, oral cortisol, both, or placebo. Intranasal insulin increased resting regional cerebral blood flow in the putamen and insular cortex, structures that are involved in the regulation of eating behavior. Neither cortisol nor interaction effects were found. These results demonstrate that insulin exerts an action in metabolic centers during resting state, which is not affected by glucocorticoids. The study described in Chapter IV uses a similar pharmacological manipulation as the one presented in Chapter III, while assessing processing of reward related food cues through the startle paradigm validated in Chapter II. A sample of men was studied during short-term food deprivation. Considering the importance of both cortisol and insulin in glucose metabolism, food pictures were divided by glycemic index. Cortisol administration enhanced ASR during foreground presentation of "high glycemic" food pictures. This result suggests that cortisol provokes an increase in reward value of high glycemic food cues, which is congruent with previous research on stress and food consumption. This thesis gives support to the FNR hypothesis towards food cues during states of deprivation. Furthermore, it highlights the potential effects of stress related hormones in metabolism-connected neuronal structures, and in the reward related mechanisms of food cue processing. In a society marked by increased food exposure and availability, alongside with increased stress, it is important to better understand the impact of food exposition and its interaction with relevant hormones. This thesis contributes to the knowledge in this field. More research in this direction is needed.