Filtern
Erscheinungsjahr
Dokumenttyp
- Dissertation (181)
- Wissenschaftlicher Artikel (30)
- Bachelorarbeit (1)
Volltext vorhanden
- ja (212) (entfernen)
Schlagworte
- Stress (33)
- Hydrocortison (15)
- stress (13)
- cortisol (12)
- Cortisol (11)
- Depression (9)
- Stressreaktion (9)
- Aufmerksamkeit (8)
- Neuroendokrines System (8)
- Psychotherapie (8)
Institut
- Psychologie (212) (entfernen)
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.
Cortisol is a stress hormone that acts on the central nervous system in order to support adaptation and time-adjusted coping processes. Whereas previous research has focused on slow emerging, genomic effects of cortisol likely mediated by protein synthesis, there is only limited knowledge about rapid, non-genomic cortisol effects on in vivo neuronal cell activity in humans. Three independent placebo-controlled studies in healthy men were conducted to test effects of 4 mg cortisol on central nervous system activity, occurring within 15 minutes after intravenous administration. Two of the studies (N = 26; N = 9) used continuous arterial spin labeling as a magnetic resonance imaging sequence, and found rapid bilateral thalamic perfusion decrements. The third study (N = 14) revealed rapid cortisol-induced changes in global signal strength and map complexity of the electroencephalogram. The observed changes in neuronal functioning suggest that cortisol may act on the thalamic relay of non-relevant background as well as on task specific sensory information in order to facilitate the adaptation to stress challenges. In conclusion, these results are the first to coherently suggest that a physiologically plausible amount of cortisol profoundly affects functioning and perfusion of the human CNS in vivo by a rapid, non-genomic mechanism.
The overall objective of this thesis was to gain a deeper understanding of the antecedents, processes, and manifestations of uniqueness-driven consumer behavior. To achieve this goal, five studies have been conducted in Germany and Switzerland with a total of 1048 participants across different demographic and socio-economic backgrounds. Two concepts were employed in all studies: Consumer need for uniqueness (CNFU) and general uniqueness perception (GUP). CNFU (Tian, Bearden, & Hunter, 2001), a mainly US"based consumer research concept, measures the individual need, and thus the motivation to acquire, use, and dispose consumer goods in order to develop a unique image. GUP, adapted from the two-component theory of individuality (Kampmeier, 2001), represents a global and direct measure of self-ascribed uniqueness. Study #1 looked at the interrelation of the uniqueness-driven concepts. Therefore, GUP and CNFU were employed in the study as potential psychological factors that influence and predict uniqueness-driven consumer behavior. Different behavioral measures were used: The newly developed possession of individualized products (POIP), the newly developed products for uniqueness display (PFUD), and the already established uniqueness-enhancing behaviors (UEB). Analyses showed that CNFU mediates the relationship between GUP and the behavioral measures in a German speaking setting. Thus, GUP (representing self-perception) was identified as the driver behind CNFU (representing motivation) and the actual consumer behavior. Study #2 examined further manifestations of uniqueness-driven consumer behavior. For this purpose, an extreme form of uniqueness-increasing behavior was researched: Tattooing. The influence of GUP and CNFU on tattooing behavior was investigated using a sample derived from a tattoo exhibition. To do so, a newly developed measure to determine the percentage of the body covered by tattoos was employed. It was revealed that individuals with higher GUP and CNFU levels indeed have a higher tattooing degree. Study #3 further explored the predictive possibilities and limitations of the GUP and CNFU concepts. On the one hand, study #3 specifically looked at the consumption of customized apparel products as mass customization is said to become the standard of the century (Piller & Müller, 2004). It was shown that individuals with higher CNFU levels not only purchased more customized apparel products in the last six months, but also spend more money on them. On the other hand, uniqueness-enhancing activities (UEA), such as travel to exotic places or extreme sports, were investigated by using a newly developed 30-item scale. It was revealed that CNFU partly mediates the GUP and UEA relationship, proving that CNFU indeed predicts a broad range of consumer behaviors and that GUP is the driver behind the need and the behavior. Study #4, entered a new terrain. In contrast to the previous three studies, it explored the so termed "passive" side of uniqueness-seeking in the consumer context. Individuals might feel unique because business companies treat them in a special way. Such a unique customer treatment (UCT) involves activities like customer service or customer relationship management. Study #4 investigated if individuals differ in their need for such a treatment. Hence, with the need for unique customer treatment (NFUCT) a new uniqueness-driven consumer need was introduced and its impact on customer loyalty examined. Analyses, for example, revealed that individuals with high NFUCT levels receiving a high unique customer treatment (UCT) showed the highest customer loyalty, whereas the lowest customer loyalty was found among those individuals with high NFUCT levels receiving a low unique customer treatment (UCT). Study #5 mainly examined the processes behind uniqueness-driven consumer behavior. Here, not only the psychological influences, but also situational influences were examined. This study investigated the impact of a non-personal "indirect" uniqueness manipulation on the consumption of customized apparel products by simultaneously controlling for the influence of GUP and CNFU. Therefore, two equal experimental groups were created. Afterwards, these groups either received an e-mail with a "pro-individualism" campaign or a "pro-collectivism" campaign especially developed for study #5. The conducted experiment revealed that, individuals receiving a "pro-individualism" poster campaign telling the participants that uniqueness is socially appropriate and desired were willing to spend more money on customization options compared to individuals receiving a "pro-collectivism" poster campaign. Hence, not only psychological antecedents such as GUP and CNFU influence uniqueness-driven consumer behavior, but also situational factors.
Die Wirksamkeit und der Nutzen von Psychotherapie sind vielfach nachgewiesen. Dennoch sind die der Psychotherapie zugrunde liegenden Wirk- und Veränderungsmechanismen zu einem großen Teil noch ungeklärt und werden kontrovers diskutiert. Ein vielversprechendes Untersuchungsdesign zur Überprüfung der Wirksamkeit und Wirkungsweise spezifischer psychotherapeutischer Techniken stellt die Untersuchung psychotherapeutischer Mikrointerventionen dar. In der vorliegenden Arbeit wurde ein laborexperimentelles Untersuchungsdesign zur Überprüfung der Wirksamkeit spezifischer psychotherapeutischer Techniken und damit einhergehender hirnphysiologischer Veränderungen erstmalig erprobt. Untersucht wurden die Effekte einer 90-minütigen psychotherapeutischen Mikrointervention, in der die Technik des kognitiven Reframings vermittelt und eingeübt wurde. Probanden einer subklinisch depressiven Stichprobe (N=45) sowie gesunde Kontrollpersonen (N=47) wurden randomisiert entweder der Mikrointervention oder einer von zwei Kontrollbedingungen zugeordnet. Die Überprüfung der interventionssezifischen Effekte erfolgte über die Erfassung ereigniskorrelierter Potenziale (EKPs) sowie Affekt-Ratings der Probanden. In einem spezifischen EEG-Paradigma wurden den Probanden negativ affektive Bilder gezeigt, die sie entweder aus einem neuen, positiven Blickwinkel betrachten oder nur anschauen sollten. Am Ende jedes Durchganges wurden die Probanden aufgefordert die Intensität ihrer emotionalen Reaktion einzuschätzen. Die Ergebnisse zeigen, dass die Psychotherapeutische Mikrointervention zu spezifischen Effekten, insbesondere auf der Ebene elektrokortikaler Veränderungen führte. Dabei wiesen die Probanden der Gruppe mit der psychotherapeutischen Mikrointervention größere mittlere frontale LPP Amplitudenwerte in Folge der Instruktionsbedingung "Umdeuten" auf. Die Ergebnisse werden im Sinne einer intensivierten kontrollierten Nutzung relevanter, über den präfrontalen Kortex vermittelter, kognitiver Verarbeitungsressourcen im Zusammenhang mit der Herunterregulierung emotionaler Reaktionen interpretiert.
During pregnancy every eighth woman is treated with glucocorticoids. Glucocorticoids inhibit cell division but are assumed to accelerate the differentiation of cells. In this review animal models for the development of the human fetal and neonatal hypothalamic-pituitary-adrenal (HPA) axis are investigated. It is possible to show that during pregnancy in humans, as in most of the here-investigated animal models, a stress hyporesponsive period (SHRP) is present. In this period, the fetus is facing reduced glucocorticoid concentrations, by low or absent fetal glucocorticoid synthesis and by reduced exposure to maternal glucocorticoids. During that phase, sensitive maturational processes in the brain are assumed, which could be inhibited by high glucocorticoid concentrations. In the SHRP, species-specific maximal brain growth spurt and neurogenesis of the somatosensory cortex take place. The latter is critical for the development of social and communication skills and the secure attachment of mother and child. Glucocorticoid treatment during pregnancy needs to be further investigated especially during this vulnerable SHRP. The hypothalamus and the pituitary stimulate the adrenal glucocorticoid production. On the other hand, glucocorticoids can inhibit the synthesis of corticotropin-releasing hormone (CRH) in the hypothalamus and of adrenocorticotropic hormone (ACTH) in the pituitary. Alterations in this negative feedback are assumed among others in the development of fibromyalgia, diabetes and factors of the metabolic syndrome. In this work it is shown that the fetal cortisol surge at the end of gestation is at least partially due to reduced glucocorticoid negative feedback. It is also assumed that androgens are involved in the control of fetal glucocorticoid synthesis. Glucocorticoids seem to prevent masculinization of the female fetus by androgens during the sexual gonadal development. In this work a negative interaction of glucocorticoids and androgens is detectable.
WICHTIGER HINWEIS: Aufgrund eines Computerfehlers bei der Rohdatenaufbereitung, müssen die 5.2.3. Ergebnisse (S. 43 ff.) wie folgt korrigiert werden: Explizite Einstellungsmessung Die Ergebnisse ändern sich inhaltlich: Haupteffekt Wortvalenz F(1, 94) = 51.10, p < .001, η2 = .35, (Mpos= 5.06; Mneg= -28.51); Interaktionseffekt Wortvalenz und kognitive Belastung F(1, 94) = 7.90, p < .01, η2 = .08, (Mpos/load= -5.01; Mpos/kein load= 15.13; Mneg/load= -25.43; Mneg/kein load= -31.75); Haupteffekt Wortnegation F(1, 94) = 8.58, p < .01, η2 = .08, (Mkeine = -7.95; Mnegation= -15.58). Implizite Einstellungsmessung Die Ergebnisse bleiben inhaltlich gleich: Zweifach-Interaktion von Wortvalenz und Prime, F(1, 80) = 4.61, p < .05, η2 = .06, (Mpos/wahr= 20.33; Mpos/falsch= 3.85; Mneg/wahr= 4.44; Mneg/falsch = 14.14). ABSTRACT: Ziel der vorliegenden Arbeit war es Evidenz für die Existenz einer Antonymie-Heuristik bei der Falsifikation valenter Information zu finden. Es wird angenommen, dass die vorherige Ankündigung, dass eine nachfolgende valenzhafte Information falsch ist, zu einer Änderung der Enkodierungsstrategie der valenzhaften Information führt. Dies bedeutet, dass zu der Valenz der gegebenen Information automatisch eine Gegenvalenz oder antonyme Valenz aktiviert werden sollte. Dementsprechend sollten falsche positive Informationen negativer und falsche negative Informationen positiver beurteilt werden als ihre wahren Entsprechungen. In vier Studien konnte dieser Effekt nachgewiesen werden. Die Ankündigung, dass eine valenzhafte Information falsch ist, beeinflusst, unabhängig von kognitiver Belastung, die Valenzübertragung in einem evaluativen Konditionierungsparadigma in vorhergesagter Weise (Experiment1). Ebenso führen generierte Gegenvalenzen, wenn eine Information als falsch angekündigt wurde, zu einem Verarbeitungsvorteil in einer Valenzkategorisierungs-Aufgabe, bei welcher positive Informationen als negativ und negative Informationen als positiv eingeschätzt werden sollten (Experiment 2). Die Ankündigung, dass eine nachfolgende Information falsch ist, führt außerdem dazu, dass positive (negative) Eigenschaften schnell und effizient negativer (positiver) eingeschätzt werden als bei einer Ankündigung der Informationen als wahr (Experiment 3 und 4). Zusammenfassend werden diese Befunde als Evidenz für die Existenz einer Antonymie-Heuristik im Zuge der Falsifikation valenter Information interpretiert.
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.
320 Probandinnen bekamen Portraitfotos von Männern und Frauen, kombiniert mit geschlechterstereotypkongruenten, -inkongruenten und -neutralen Eigenschaften unter verschiedenen Instruktions- und Rahmenbedingungen vorgelegt. Anschließend erfolgten, für Items und Assoziationen, explizite Gedächtnistests. Die Ergebnisse belegen einen wiederholten assoziativen Inkongruenzvorteil, stereotypkongruente Rateverzerrungen, ein moderierendes individuelles Stereotypizitätsniveau, Ausbleiben stereotypkongruenten Einflusses nach intentionaler Instruktion, die Interaktion von Gedächtnisleistung und instruktionsvermittelnder Fokussierung, einen Erinnerungsvorteil für assoziative im Vergleich zu Iteminformationen sowie Leistungsminderung bei paralleler Aufmerksamkeitsbelastung. In der zeitunbegrenzten Testphase bwz. der Erfassung der probandeneigenen Reaktionszeiten wird eine wichtige Aufklärungsquelle vermutet.
Stress and pain are common experiences in human lives. Both, the stress and the pain system have adaptive functions and try to protect the organism in case of harm and danger. However, stress and pain are two of the most challenging problems for the society and the health system. Chronic stress, as often seen in modern societies, has much impact on health and can lead to chronic stress disorders. These disorders also include a number of chronic pain syndromes. However, pain can also be regarded as a stressor itself, especially when we consider how much patients suffer from long-lasting pain and the impact of pain on life quality. In this way, the effects of stress on pain can be fostered. For the generation and manifestation of chronic pain symptoms also learning processes such as classical conditioning play an important role. Processes of classical conditioning can also be influenced by stress. These facts illustrate the complex and various interactions between the pain and the stress systems. Both systems communicate permanently with each other and help to protect the organism and to keep a homeostatic state. They have various ways of communication, for example mechanisms related to endogenous opioids, immune parameters, glucocorticoids and baroreflexes. But an overactivation of the systems, for example caused by ongoing stress, can lead to severe health problems. Therefore, it is of great importance to understand these interactions and their underlying mechanisms. The present work deals with the relationship of stress and pain. A special focus is put on stress related hypocortisolism and pain processing, stress induced hypoalgesia via baroreceptor related mechanisms and stress related cortisol effects on aversive conditioning (as a model of pain learning). This work is a contribution to the wide field of research that tries to understand the complex interactions of stress and pain. To demonstrate the variety, the selected studies highlight different aspects of these interactions. In the first chapter I will give a short introduction on the pain and the stress systems and their ways of interaction. Furthermore, I will give a short summary of the studies presented in Chapter II to V and their background. The results and their meaning for future research will be discussed in the last part of the first chapter. Chronic pain syndromes have been associated with chronic stress and alterations of the HPA axis resulting in chronic hypocortisolism. But if these alterations may play a causal role in the pathophysiology of chronic pain remains unclear. Thus, the study described in Chapter II investigated the effects of pharmacological induced hypocortisolism on pain perception. Both, the stress and the pain system are related to the cardiovascular system. Increase of blood pressure is part of the stress reaction and leads to reduced pain perception. Therefore, it is important for the usage of pain tests to keep in mind potential interferences from activation of the cardiovascular system, especially when pain inhibitory processes are investigated. For this reason we compared two commonly and interchangeably used pain tests with regard to the triggered autonomic reactions. This study is described in chapter III. Chapter IV and V deal with the role of learning processes in pain and related influences of stress. Processes of classical conditioning play an important role for symptom generation and manifestation. In both studies aversive eyeblink conditioning was used as a model for pain learning. In the study described in Chapter IV we compared classical eyeblink conditioning in healthy volunteers to patients suffering from fibromyalgia, a chronic pain disorder. Also, differences of the HPA axis, as part of the stress system, were taken in account. The study of Chapter V investigated effects of the very first stress reaction, particularly rapid non-genomic cortisol effects. Healthy volunteers received an intravenous cortisol administration immediately before the eyeblink conditioning. Rapid effects have only been demonstrated on a cellular level and on animal behavior so far. In general, the studies presented in this work may give an impression of the broad variety of possible interactions between the pain and the stress system. Furthermore, they contribute to our knowledge about theses interactions. However, more research is needed to complete the picture.
In this thesis, three studies investigating the impact of stress on the protective startle eye blink reflex are reported. In the first study a decrease in prepulse inhibition of the startle reflex was observed after intravenous low dose cortisol application. In the second study a decrease in reflex magnitude of the startle reflex was observed after pharmacological suppression of endogenous cortisol production. In the third study, a higher reflex magnitude of the startle reflex was observed at reduced arterial and central venous blood pressure. These results can be interpreted in terms of an adaption to hostile environments.