TY - JOUR A1 - Bonn, M. A1 - Schmitt, A. A1 - Lesch, K.-P. A1 - Van Bockstaele, E. J. A1 - Asan, E. T1 - Serotonergic innervation and serotonin receptor expression of NPY-producing neurons in the rat lateral and basolateral amygdaloid nuclei JF - Brain Structure and Function N2 - Pharmacobehavioral studies in experimental animals, and imaging studies in humans, indicate that serotonergic transmission in the amygdala plays a key role in emotional processing, especially for anxiety-related stimuli. The lateral and basolateral amygdaloid nuclei receive a dense serotonergic innervation in all species studied to date. We investigated interrelations between serotonergic afferents and neuropeptide Y (NPY)-producing neurons, which are a subpopulation of inhibitory interneurons in the rat lateral and basolateral nuclei with particularly strong anxiolytic properties. Dual light microscopic immunolabeling showed numerous appositions of serotonergic afferents on NPY-immunoreactive somata. Using electron microscopy, direct membrane appositions and synaptic contacts between serotonin-containing axon terminals and NPY-immunoreactive cellular profiles were unequivocally established. Double in situ hybridization documented that more than 50 %, and about 30–40 % of NPY mRNA-producing neurons, co-expressed inhibitory 5-HT1A and excitatory 5-HT2C mRNA receptor subtype mRNA, respectively, in both nuclei with no gender differences. Triple in situ hybridization showed that individual NPY mRNA-producing interneurons co-express both 5-HT1A and 5-HT2C mRNAs. Co-expression of NPY and 5-HT3 mRNA was not observed. The results demonstrate that serotonergic afferents provide substantial innervation of NPY-producing neurons in the rat lateral and basolateral amygdaloid nuclei. Studies of serotonin receptor subtype co-expression indicate a differential impact of the serotonergic innervation on this small, but important, population of anxiolytic interneurons, and provide the basis for future studies of the circuitry underlying serotonergic modulation of emotional stimulus processing in the amygdala. KW - NPY KW - serotonergic system KW - amygdala KW - anxiety Y1 - 2013 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-132591 VL - 218 IS - 2 ER - TY - JOUR A1 - Buff, Christine A1 - Brinkmann, Leonie A1 - Bruchmann, Maximilian A1 - Becker, Michael P.I. A1 - Tupak, Sara A1 - Herrmann, Martin J. A1 - Straube, Thomas T1 - Activity alterations in the bed nucleus of the stria terminalis and amygdala during threat anticipation in generalized anxiety disorder JF - Social Cognitive and Affective Neuroscience N2 - Sustained anticipatory anxiety is central to Generalized Anxiety Disorder (GAD). During anticipatory anxiety, phasic threat responding appears to be mediated by the amygdala, while sustained threat responding seems related to the bed nucleus of the stria terminalis (BNST). Although sustained anticipatory anxiety in GAD patients was proposed to be associated with BNST activity alterations, firm evidence is lacking. We aimed to explore temporal characteristics of BNST and amygdala activity during threat anticipation in GAD patients. Nineteen GAD patients and nineteen healthy controls (HC) underwent functional magnetic resonance imaging (fMRI) during a temporally unpredictable threat anticipation paradigm. We defined phasic and a systematic variation of sustained response models for blood oxygen level-dependent responses during threat anticipation, to disentangle temporally dissociable involvement of the BNST and the amygdala. GAD patients relative to HC responded with increased phasic amygdala activity to onset of threat anticipation and with elevated sustained BNST activity that was delayed relative to the onset of threat anticipation. Both the amygdala and the BNST displayed altered responses during threat anticipation in GAD patients, albeit with different time courses. The results for the BNST activation hint towards its role in sustained threat responding, and contribute to a deeper understanding of pathological sustained anticipatory anxiety in GAD. KW - medicine KW - anticipatory anxiety KW - anxiety KW - fMRI KW - sustained threat responding KW - phasic threat responding Y1 - 2017 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-173298 VL - 12 IS - 11 ER - TY - JOUR A1 - Diemer, Julia A1 - Alpers, Georg W. A1 - Peperkorn, Henrik M. A1 - Shiban, Youssef A1 - Mühlberger, Andreas T1 - The impact of perception and presence on emotional reactions: a review of research in virtual reality JF - Frontiers in Psychology N2 - Virtual reality (VR) has made its way into mainstream psychological research in the last two decades. This technology, with its unique ability to simulate complex, real situations and contexts, offers researchers unprecedented opportunities to investigate human behavior in well controlled designs in the laboratory. One important application of VR is the investigation of pathological processes in mental disorders, especially anxiety disorders. Research on the processes underlying threat perception, fear, and exposure therapy has shed light on more general aspects of the relation between perception and emotion. Being by its nature virtual, i.e., simulation of reality, VR strongly relies on the adequate selection of specific perceptual cues to activate emotions. Emotional experiences in turn are related to presence, another important concept in VR, which describes the user's sense of being in a VR environment. This paper summarizes current research into perception of fear cues, emotion, and presence, aiming at the identification of the most relevant aspects of emotional experience in VR and their mutual relations. A special focus lies on a series of recent experiments designed to test the relative contribution of perception and conceptual information on fear in VR. This strand of research capitalizes on the dissociation between perception (bottom up input) and conceptual information (top-down input) that is possible in VR. Further, we review the factors that have so far been recognized to influence presence, with emotions (e.g., fear) being the most relevant in the context of clinical psychology. Recent research has highlighted the mutual influence of presence and fear in VR, but has also traced the limits of our current understanding of this relationship. In this paper, the crucial role of perception on eliciting emotional reactions is highlighted, and the role of arousal as a basic dimension of emotional experience is discussed. An interoceptive attribution model of presence is suggested as a first step toward an integrative framework for emotion research in VR. Gaps in the current literature and future directions are outlined. KW - exposure therapy KW - flight phobics KW - environments KW - virtual reality KW - anxiety KW - presence KW - emotion KW - fear KW - perception KW - anxiety disorders KW - presence questionnaire KW - public speaking KW - spider phobia KW - social phobia KW - immersion Y1 - 2015 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-144200 VL - 6 IS - 26 ER - TY - JOUR A1 - Eisele, Marion A1 - Blozik, Eva A1 - Störk, Stefan A1 - Träder, Jens-Martin A1 - Herrmann-Lingen, Christoph A1 - Scherer, Martin T1 - Recognition of depression and anxiety and their association with quality of life, hospitalization and mortality in primary care patients with heart failure - study protocol of a longitudinal observation study JF - BMC Family Practice N2 - Background: International disease management guidelines recommend the regular assessment of depression and anxiety in heart failure patients. Currently there is little data on the effect of screening for depression and anxiety on the quality of life and the prognosis of heart failure (HF). We will investigate the association between the recognition of current depression/anxiety by the general practitioner (GP) and the quality of life and the patients' prognosis. Methods/Design: In this multicenter, prospective, observational study 3,950 patients with HF are recruited by general practices in Germany. The patients fill out questionnaires at baseline and 12-month follow-up. At baseline the GPs are interviewed regarding the somatic and psychological comorbidities of their patients. During the follow-up assessment, data on hospitalization and mortality are provided by the general practice. Based on baseline data, the patients are allocated into three observation groups: HF patients with depression and/or anxiety recognized by their GP (P+/+), those with depression and/or anxiety not recognized (P+/-) and patients without depression and/or anxiety (P-/-). We will perform multivariate regression models to investigate the influence of the recognition of depression and/or anxiety on quality of life at 12 month follow-up, as well as its influences on the prognosis (hospital admission, mortality). Discussion: We will display the frequency of GP-acknowledged depression and anxiety and the frequency of installed therapeutic strategies. We will also describe the frequency of depression and anxiety missed by the GP and the resulting treatment gap. Effects of correctly acknowledged and missed depression/anxiety on outcome, also in comparison to the outcome of subjects without depression/anxiety will be addressed. In case results suggest a treatment gap of depression/anxiety in patients with HF, the results of this study will provide methodological advice for the efficient planning of further interventional research. KW - anxiety KW - depression KW - health care research KW - heart failure KW - prevalence KW - observational study KW - prognosis KW - quality of life KW - hospitalization KW - treatment KW - mortality KW - task force KW - health questionnaire KW - cardiovascular care KW - validity KW - scale KW - validation KW - outcomes KW - standardization KW - population Y1 - 2013 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-121881 SN - 1471-2296 VL - 14 IS - 180 ER - TY - JOUR A1 - Esser, Peter A1 - Mehnert‐Theuerkauf, Anja A1 - Friedrich, Michael A1 - Johansen, Christoffer A1 - Brähler, Elmar A1 - Faller, Hermann A1 - Härter, Martin A1 - Koch, Uwe A1 - Schulz, Holger A1 - Wegscheider, Karl A1 - Weis, Joachim A1 - Kuba, Katharina A1 - Hinz, Andreas A1 - Hartung, Tim T1 - Risk and associated factors of depression and anxiety in men with prostate cancer: Results from a German multicenter study JF - Psycho‐Oncology N2 - Objective In order to optimize psycho‐oncological care, studies that quantify the extent of distress and identify certain risk groups are needed. Among patients with prostate cancer (PCa), findings on depression and anxiety are limited. Methods We analyzed data of PCa patients selected from a German multi‐center study. Depression and anxiety were assessed with the PHQ‐9 and the GAD‐7 (cut‐off ≥7). We provided physical symptom burden, calculated absolute and relative risk (AR and RR) of depression and anxiety across patient subsets and between patients and the general population (GP) and tested age as a moderator within the relationship of disease‐specific symptoms with depression and anxiety. Results Among 636 participants, the majority reported disease‐specific problems (sexuality: 60%; urination: 52%). AR for depression and anxiety was 23% and 22%, respectively. Significant RR were small, with higher risks of distress in patients who are younger (eg, RR\(_{depression}\) = 1.15; 95%‐CI: 1.06‐1.26), treated with chemotherapy (RR\(_{depression}\)n = 1.46; 95%‐CI: 1.09‐1.96) or having metastases (RR\(_{depression}\) = 1.30; 95%‐CI: 1.02‐1.65). Risk of distress was slightly elevated compared to GP (eg, RR\(_{depression}\) = 1.13; 95%‐CI: 1.07‐1.19). Age moderated the relationship between symptoms and anxiety (B\(_{urination}\) = −0.10, P = .02; B\(_{sexuality}\) = −0.11, P = .01). Conclusions Younger patients, those with metastases or treatment with chemotherapy seem to be at elevated risk for distress and should be closely monitored. Many patients suffer from disease‐specific symptom burden, by which younger patients seem to be particularly distressed. Support of coping mechanisms associated with disease‐specific symptom burden seems warranted. KW - anxiety KW - cancer KW - depression KW - oncology KW - prostatic neoplasms Y1 - 2020 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-218277 VL - 29 IS - 10 SP - 1604 EP - 1612 ER - TY - JOUR A1 - Frey, Anna A1 - Popp, Sandy A1 - Post, Antonia A1 - Langer, Simon A1 - Lehmann, Marc A1 - Hofmann, Ulrich A1 - Siren, Anna-Leena A1 - Hommers, Leif A1 - Schmitt, Angelika A1 - Strekalova, Tatyana A1 - Ertl, Georg A1 - Lesch, Klaus-Peter A1 - Frantz, Stefan T1 - Experimental heart failure causes depression-like behavior together with differential regulation of inflammatory and structural genes in the brain JF - Frontiers in Behavioral Neuroscience N2 - Background: Depression and anxiety are common and independent outcome predictors in patients with chronic heart failure (CHF). However, it is unclear whether CHF causes depression. Thus, we investigated whether mice develop anxiety- and depression-like behavior after induction of ischemic CHF by myocardial infarction (MI). Methods and Results: In order to assess depression-like behavior, anhedonia was investigated by repeatedly testing sucrose preference for 8 weeks after coronary artery ligation or sham operation. Mice with large MI and increased left ventricular dimensions on echocardiography (termed CHF mice) showed reduced preference for sucrose, indicating depression-like behavior. 6 weeks after MI, mice were tested for exploratory activity, anxiety-like behavior and cognitive function using the elevated plus maze (EPM), light-dark box (LDB), open field (OF), and object recognition (OR) tests. In the EPM and OF, CHF mice exhibited diminished exploratory behavior and motivation despite similar movement capability. In the OR, CHF mice had reduced preference for novelty and impaired short-term memory. On histology, CHF mice had unaltered overall cerebral morphology. However, analysis of gene expression by RNA-sequencing in prefrontal cortical, hippocampal, and left ventricular tissue revealed changes in genes related to inflammation and cofactors of neuronal signal transduction in CHF mice, with Nr4a1 being dysregulated both in prefrontal cortex and myocardium after MI. Conclusions: After induction of ischemic CHF, mice exhibited anhedonic behavior, decreased exploratory activity and interest in novelty, and cognitive impairment. Thus, ischemic CHF leads to distinct behavioral changes in mice analogous to symptoms observed in humans with CHF and comorbid depression. KW - chronic heart failure KW - myocardial infarction KW - anxiety KW - depression KW - mice Y1 - 2014 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-118234 SN - 1662-5153 VL - 8 ER - TY - JOUR A1 - Geis, Christian A1 - Weishaupt, Andreas A1 - Grünewald, Benedikt A1 - Wultsch, Thomas A1 - Reif, Andreas A1 - Gerlach, Manfred A1 - Dirkx, Ron A1 - Solimena, Michele A1 - Toyka, Klaus V A1 - Folli, Franco A1 - Perani, Daniela A1 - Heckmann, Manfred A1 - Sommer, Claudia T1 - Human Stiff-Person Syndrome IgG Induces Anxious Behavior in Rats JF - Plos One N2 - Background: Anxiety is a heterogeneous behavioral domain playing a role in a variety of neuropsychiatric diseases. While anxiety is the cardinal symptom in disorders such as panic disorder, co-morbid anxious behavior can occur in a variety of diseases. Stiff person syndrome (SPS) is a CNS disorder characterized by increased muscle tone and prominent agoraphobia and anxiety. Most patients have high-titer antibodies against glutamate decarboxylase (GAD) 65. The pathogenic role of these autoantibodies is unclear. Methodology/Principal Findings: We re-investigated a 53 year old woman with SPS and profound anxiety for GABA-A receptor binding in the amygdala with (11) C-flumazenil PET scan and studied the potential pathogenic role of purified IgG from her plasma filtrates containing high-titer antibodies against GAD 65. We passively transferred the IgG fraction intrathecally into rats and analyzed the effects using behavioral and in vivo electrophysiological methods. In cell culture, we measured the effect of patient IgG on GABA release from hippocampal neurons. Repetitive intrathecal application of purified patient IgG in rats resulted in an anxious phenotype resembling the core symptoms of the patient. Patient IgG selectively bound to rat amygdala, hippocampus, and frontal cortical areas. In cultured rat hippocampal neurons, patient IgG inhibited GABA release. In line with these experimental results, the GABA-A receptor binding potential was reduced in the patient's amygdala/hippocampus complex. No motor abnormalities were found in recipient rats. Conclusion/Significance: The observations in rats after passive transfer lead us to propose that anxiety-like behavior can be induced in rats by passive transfer of IgG from a SPS patient positive for anti-GAD 65 antibodies. Anxiety, in this case, thus may be an antibody-mediated phenomenon with consecutive disturbance of GABAergic signaling in the amygdala region. KW - Glutamic-acid decarboxylase anxiety KW - spinal-cord-injury KW - presynaptic inhibition KW - 65-kda isoform KW - fear memory KW - antibodies KW - disorder KW - neurons KW - anxiety KW - autoantibodies Y1 - 2011 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-140506 VL - 6 IS - 2 ER - TY - THES A1 - Glotzbach-Schoon, Evelyn T1 - Contextual fear conditioning in humans: The return of contextual anxiety and the influence of genetic polymorphisms T1 - Kontextuelle Furchtkonditionierung beim Menschen: die Wiederkehr von Kontextangst und der Einfluss von genetischen Polymorphismen N2 - Als Angst bezeichnet man einen nicht auf spezifische Objekte gerichteten länger anhaltenden zukunfts-orientierten Zustand der Besorgnis. Diese ist kennzeichnend für Angststörungen wie Panikstörung, generalisierte Angststörung und Posttraumatische Belastungsstörung (PTBS). Experimentell kann Angst durch kontextuelle Furchtkonditionierung ausgelöst werden. Bei dieser Art der Konditionierung werden aversive Ereignisse als unvorhersehbar erlebt, wodurch der gesamte Kontext mit der Gefahr assoziiert wird. Diese Arbeit hat zum Ziel, Mechanismen der Entstehung und Aufrechterhaltung von Kontextangst zu untersuchen. Dies sind zum einem erleichterte Akquisition von Kontextkonditionierungen und deren fehlerhafte Extinktion. Hier ist vor allem die Fragestellung relevant, wie dies durch genetische Varianten moduliert wird (Studie 1). Zum anderen soll die Wiederkehr der Angst nach der Extinktion mit einem neuen Reinstatement-Paradigma untersucht werden (Studie 2). Zur Untersuchung dieser Forschungsfragen wurden zwei kontextuelle Furchtkonditionierungsstudien in virtueller Realität (VR) durchgeführt. Während der Akquisition wurden leicht schmerzhafte elektrische Reize (unkonditionierter Stimulus, US) unvorhersehbar präsentiert, während die Probanden in einem virtuellen Büroraum waren. Dadurch wurde dieser Raum zum Angstkontext (CXT+). Ein zweiter Büroraum wurde nie mit dem US gepaart, deshalb wurde dieser Raum zum Sicherheitskontext (CXT-). Die Extinktion, in der die Kontexte ohne US präsentiert wurden, fand 24 h später statt, und ein Test zum Abruf der Extinktion bzw. zur Wiederkehr der Angst nochmals 24 h später. In beiden Studien wurde die Angst auf drei verschiedenen Ebenen gemessen: Verhalten (angstpotenzierter Schreckreflex), Physiologie (tonische Hautleitfähigkeit), und verbale Ebene (explizite Ratings). Die Probanden für Studie 1 wurden anhand der 5-HTTLPR (S+ Risikoallel vs. LL nicht-Risikoallel) und NPSR1 rs324981 (T+ Risikoallel vs. AA nicht-Risikoallel) Polymorphismen stratifiziert, sodass vier kombinierte Genotyp Gruppen (S+/T+, S+/LL, LL/T+ und LL/AA) mit je 20 Probanden vorlagen. Es zeigte sich, dass der angstpotenzierte Schreckreflex durch die Interaktion zwischen beiden genetischen Polymorphismen moduliert wurde. Nur Träger beider Risikoallele (S+ Träger des 5-HTTLPR und T+ Träger des NPSR1 Polymorphismus) zeigten einen höheren Schreckreflex im CXT+ als im CXT- während der Akquisition. Der Abruf der Extinktion an Tag 3, gemessen anhand des Schreckreflexes, wurde allerdings nicht durch die Genotypen moduliert. Interessanterweise zeigte sich auf dem expliziten Angstlevel (Valenz- und Angstratings) nur ein Einfluss des NPSR1 Polymorphismus, und zwar bewerteten die nicht-Risikoallel Träger (AA) den CXT+ mit negativerer Valenz und höherer Angst im Vergleich zum CXT-; die Risikoallel Träger (T+) taten dies nicht. In der zweiten Studie wurde fast das gleiche Paradigma benutzt wie in der ersten Studie mit der Ausnahme, dass eine Versuchsgruppe (Reinstatementgruppe) den US noch einmal am Anfang des dritten Untersuchungstages vor der Präsentation von CXT+ und CXT- appliziert bekam. Die zweite Versuchsgruppe (Kontrollgruppe) erhielt keinen US, sondern wurde direkt durch CXT+ und CXT- geführt. Es zeigte sich, dass nur in der Reinstatementgruppe die Angst auf impliziter und expliziter Ebene wiederkehrte, d.h. die Probanden zeigten einen höheren Schreckreflex und höhere Angstratings auf den CXT+ im Vergleich zum CXT-. Wichtig war vor allem, dass die Wiederkehr der Angst in der Reinstatementgruppe mit der Veränderung der Zustandsangst und der Stimmung (von der Extinktion zum Test) korrelierte. D.h. je größer die Angst und je negativer die Stimmung wurden, desto höher war die Wiederkehr der Angst. Zusammengefasst belegt Studie 1, dass erleichterte kontextuelle Furchtkonditionierung auf impliziter Ebene (Schreckreflex) ein Endophänotyp für Angststörungen sein könnte, was zu unserem Verständnis der Ätiologie von Angststörungen beitragen könnte. Die Ergebnisse der zweiten Studie legen nahe, dass eine ängstliche und negative Stimmung nach der Extinktion die Rückkehr von Angst begünstigen könnte. Darüber hinaus scheint das VR-basierte kontextuelle Furchtkonditionierungsparadigma ein geeignetes Mittel zu sein, um Mechanismen der Angstentstehung und Angstwiederkehr experimentell zu erforschen. Weiterführende Studien könnten nun auch Angstpatienten untersuchen und das Paradigma auf evolutionär-relevante Kontexte (z.B. Höhe, Dunkelheit, weite Plätze) ausweiten. N2 - Sustained anxiety is considered as a chronic and future-oriented state of apprehension that does not belong to a specific object. It is discussed as an important characteristic of anxiety disorders including panic disorder, generalized anxiety disorder (GAD) and posttraumatic stress disorder (PTSD). Experimentally, sustained anxiety can be induced by contextual fear conditioning in which aversive events are unpredictably presented and therefore the whole context becomes associated with the threat. This thesis aimed at investigating important mechanisms in the development and maintenance of sustained anxiety: (1) facilitated acquisition and resistant extinction of contextual anxiety due to genetic risk factors (Study 1), and (2) the return of contextual anxiety after successful extinction using a new reinstatement paradigm (Study 2). To this end, two contextual fear conditioning studies were conducted in virtual reality (VR). During acquisition one virtual office was paired with unpredictable mildly painful electric stimuli (unconditioned stimulus, US), thus becoming the anxiety context (CXT+). Another virtual office was never paired with any US, thus becoming the safety context (CXT-). Extinction was conducted 24 h later, i.e. no US was presented, and extinction recall was tested another 24 h later on Day 3. In both studies context-evoked anxiety was measured on three different response levels: behavioral (anxiety-potentiated startle reflex), physiological (skin conductance level), and verbal (explicit ratings). In Study 1, participants were stratified for 5-HTTLPR (S+ risk allele vs. LL no risk allele) and NPSR1 rs324981 (T+ risk allele vs. AA no risk allele) polymorphisms, resulting in four combined genotype groups with 20 participants each: S+/T+, S+/LL, LL/T+, and LL/AA. Results showed that acquisition of anxiety-potentiated startle was influenced by a gene × gene interaction: only carriers of both risk alleles (S+ carriers of the 5-HTTLPR and T+ carriers of the NPSR1 polymorphism) exhibited significantly higher startle magnitudes in CXT+ compared to CXT-. However, extinction recall as measured with anxiety-potentiated startle was not affected by any genotype. Interestingly, the explicit anxiety level, i.e. valence and anxiety ratings, was only influenced by the NPSR1 genotype, in a way that no risk allele carriers (AA) reported higher anxiety and more negative valence in response to CXT+ compared to CXT-, whereas risk allele carriers (T+) did not. Study 2 adopted nearly the same paradigm with the modification that one group (reinstatement group) received one unsignaled US at the beginning of the experimental session on Day 3 before seeing CXT+ and CXT-. The second group served as a control group and received no US, but was immediately exposed to CXT+ and CXT-. Results showed a return of anxiety on the implicit and explicit level (higher startle responses and anxiety ratings in response to CXT+ compared to CXT-) in the reinstatement group only. Most important, the return of contextual anxiety in the reinstatement group was associated with a change of state anxiety and mood from extinction to test, that is the more anxiety and negative mood participants experienced before the reinstatement procedure, the higher their return of anxiety was. In sum, results of Study 1 showed that facilitated contextual fear conditioning on an implicit behavioral level (startle response) could be regarded as an endophenotype for anxiety disorders, which can contribute to our understanding of the etiology of anxiety disorders. Results of Study 2 imply that anxiety and negative mood after extinction could be an important facilitator for the return of anxiety. Furthermore, the present VR-based contextual fear conditioning paradigm seems to be an ideal tool to experimentally study mechanisms underlying the acquisition and the return of anxiety. Future studies could investigate clinical samples and extend the VR paradigm to evolutionary-relevant contexts (e.g., heights, darkness, open spaces). KW - Angst KW - Genetik KW - Kontextkonditionierung KW - context conditioning KW - anxiety KW - genetics KW - virtual reality KW - Virtuelle Realität Y1 - 2013 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-87955 ER - TY - JOUR A1 - Gromer, Daniel A1 - Kiser, Dominik P. A1 - Pauli, Paul T1 - Thigmotaxis in a virtual human open field test JF - Scientific Reports N2 - Animal models are used to study neurobiological mechanisms in mental disorders. Although there has been significant progress in the understanding of neurobiological underpinnings of threat-related behaviors and anxiety, little progress was made with regard to new or improved treatments for mental disorders. A possible reason for this lack of success is the unknown predictive and cross-species translational validity of animal models used in preclinical studies. Re-translational approaches, therefore, seek to establish cross-species translational validity by identifying behavioral operations shared across species. To this end, we implemented a human open field test in virtual reality and measured behavioral indices derived from animal studies in three experiments (N=31, N=30, and N=80). In addition, we investigated the associations between anxious traits and such behaviors. Results indicated a strong similarity in behavior across species, i.e., participants in our study-like rodents in animal studies-preferred to stay in the outer region of the open field, as indexed by multiple behavioral parameters. However, correlational analyses did not clearly indicate that these behaviors were a function of anxious traits of participants. We conclude that the realized virtual open field test is able to elicit thigmotaxis and thus demonstrates cross-species validity of this aspect of the test. Modulatory effects of anxiety on human open field behavior should be examined further by incorporating possible threats in the virtual scenario and/or by examining participants with higher anxiety levels or anxiety disorder patients. KW - anxiety KW - human behavior KW - anciety-like behavior KW - approach-avoidance conflict KW - elevated plus-maze KW - spatial navigation KW - mental disorders KW - fear KW - threat KW - circuits KW - reality KW - metaanalysis Y1 - 2021 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-259850 VL - 11 ER - TY - JOUR A1 - Gromer, Daniel A1 - Madeira, Octávia A1 - Gast, Philipp A1 - Nehfischer, Markus A1 - Jost, Michael A1 - Müller, Mathias A1 - Mühlberger, Andreas A1 - Pauli, Paul T1 - Height Simulation in a Virtual Reality CAVE System: Validity of Fear Responses and Effects of an Immersion Manipulation JF - Frontiers in Human Neuroscience N2 - Acrophobia is characterized by intense fear in height situations. Virtual reality (VR) can be used to trigger such phobic fear, and VR exposure therapy (VRET) has proven effective for treatment of phobias, although it remains important to further elucidate factors that modulate and mediate the fear responses triggered in VR. The present study assessed verbal and behavioral fear responses triggered by a height simulation in a 5-sided cave automatic virtual environment (CAVE) with visual and acoustic simulation and further investigated how fear responses are modulated by immersion, i.e., an additional wind simulation, and presence, i.e., the feeling to be present in the VE. Results revealed a high validity for the CAVE and VE in provoking height related self-reported fear and avoidance behavior in accordance with a trait measure of acrophobic fear. Increasing immersion significantly increased fear responses in high height anxious (HHA) participants, but did not affect presence. Nevertheless, presence was found to be an important predictor of fear responses. We conclude that a CAVE system can be used to elicit valid fear responses, which might be further enhanced by immersion manipulations independent from presence. These results may help to improve VRET efficacy and its transfer to real situations. KW - anxiety KW - fear behavior KW - virtual reality KW - presence KW - immersion KW - acrophobia Y1 - 2018 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-196113 SN - 1662-5161 VL - 12 IS - 372 ER -