Inhalt 1 INHALT HAUPTREDNER / KEYNOTE LECTURES (HS 3)............................................................................................ 2 SYMPOSIEN ............................................................................................................................................................................ 3 SYMPOSIEN DONNERSTAG 08:30–10:00 ............................................................................................................ 3 SYMPOSIEN DONNERSTAG 11:30-13:00 ........................................................................................................... 10 SYMPOSIEN DONNERSTAG 16:00-17:30 ........................................................................................................... 14 SYMPOSIEN FREITAG 08:30-10:00........................................................................................................................ 23 SYMPOSIEN FREITAG 11:30-13:00........................................................................................................................ 29 SYMPOSIEN FREITAG 16:30-18:00........................................................................................................................ 35 SYMPOSIEN SAMSTAG 09:00-10:30 ..................................................................................................................... 44 SYMPOSIEN SAMSTAG 12:00-13:30 ..................................................................................................................... 48 POSTERSESSIONS ........................................................................................................................................................... 55 Postersession Donnerstag (Posternummern 01 – 44) ................................................................................... 55 Postersession Donnerstag (Posternummern 45 – 88) ................................................................................... 71 Postersession Freitag (Posternummern 01 – 44) .......................................................................................... 88 Postersession Freitag (Posternummern 45 – 88) ....................................................................................... 103 POSTERBLITZ DER JUNGWISSENSCHAFTLER 2017 .......................................................................... 119 PERSONENVERZEICHNIS ........................................................................................................................................ 123 2 Keynote Lectures | PuG Trier 2017 HAUPTREDNER / KEYNOTE LECTURES (HS 3) DONNERSTAG, 15. JUNI 2017, 10:40 – 11:30 What we know (and do not know) about prepulse inhibition of startle Terry D. Blumenthal - Wake Forest University, Winston-Salem, NC USA The startle reflex is a phylogenetically old and very sensitive constellation of responses that serve both defensive and interruptive properties. Startle can be measured in a range of animal models, and in humans across the lifespan. This response is very sensitive to variations in stimulus and situational parameters, personality characteristics, clinical diagnoses, and pharmacological, social, and cognitive situations. One intriguing property of startle is the fact that it can be profoundly inhibited by the presentation of an otherwise innocuous stimulus, called a prepulse, shortly before the startle stimulus. This prepulse inhibition (PPI) of startle is a very reliable and robust effect, attenuating the startle response completely in many cases. PPI can vary based on a multitude of stimulus, situation, and person parameters, and some of those factors will be discussed in this presenta- tion. Information about the sensitivity and utility of PPI will also be provided, suggesting applications in a variety of areas in psychology and neurosci- ence. An effort will also be made to correct some misconceptions about PPI, and to point toward future developments in the application of this exceedingly sensitive and useful measure. FREITAG, 16. JUNI 2017, 10:40 – 11:30 Lernen, Gedächtnis und Plastizität des Gehirns: Implikationen für Verhaltensänderung Herta Flor - Zentralinstitut für Seelische Gesundheit, Mannheim Lern- und Gedächtnisprozesse und damit einhergehende maladaptive plastische Veränderungen des Gehirns spielen bei der Entstehung psychischer Störungen, und spezifisch bei chronischen Schmerzen, eine entscheidende Rolle. Dabei dürfte das Hauptproblem die Unfähigkeit sein, aversive Gedächtnisinhalte zu löschen, die sowohl explizite wie auch implizite Gedächtnisspuren umfassen. Der dominante psychologische Zugang zu diesen Störungen ist kognitiv-verhaltenstherapeutisch. Jedoch fokussieren diese Trainings auf eine Verminderung von Einschränkungen und die Bildung von Bewältigungsfertigkeiten. Auf der Basis der Evidenz für Gedächtnisprozesse in der Psychopathologie könnten hirnbasierte Extinktionsverfahren und sensomotorische Trainings alternative und eher an den Mechanismen orientierte Behandlungsalternativen für emotionale und sensorische Störun- gen sein, die durch extinktionsfördernde pharmakologische Interventionen verstärkt werden können. Wenn Personen lernen können, spezifische Hirnregionen zu beeinflussen, so hat das auch Implikationen für periphere Prozesse wie die Muskelspannung oder für die Körperwahrnehmung. Somit lassen sich diese Prinzipien auch auf die Behandlung von Immobilität nach Verletzungen oder chronischen Krankheiten sowie pathologische Altersprozesse wie Gebrechlichkeit oder Demenz übertragen. Dabei sind motivationale Aspekte besonders wichtig, die sich durch virtuelle Realität und Spielumgebungen realisieren lassen. Mit Unterstützung von SFB636 (Psychopathologie), SFB1158 (Thema Schmerz) und einem Reinhart-Koselleck-Projekt der Deutschen Forschungs- gemeinschaft. SAMSTAG, 17. JUNI 2017, 11:00 – 12:00 Bidirectional effects of early life adversity on stress system regulation – in search for a comprehensive theory Jens Prüssner - Universität Konstanz Early life adversity (ELA), in the form of low parental care or overprotection, or physical, sexual, or emotional abuse, is consistently linked to poor mental health outcomes in adulthood, including psychosis, depression, and burnout. A generally agreed-upon mediator of these effects is a changed regulation of the stress /energy systems in the organism, namely the autonomic nervous system (ANS), and the hypothalamic-pituitary adrenal (hpa) axis. Investigated in both human and animal studies, these systems are consistently found dysregulated in organisms exposed to ELA, however the directionality is unclear, with some studies demonstrating heightened activity, while others show blunting of the biomarkers of the system, after exposure to adversity early in life. Several theories exist that try to explain these mixed effects, considering factors like age of exposure, trauma severity, duration, or type. Importantly, none of the theories can be used to explain all of the available data, suggesting that additional factors / mediators might be at play. The current talk will summarize the major theories in the field and point out some of the commonalities and differences among them. In addition, it will introduce potential mediators that are currently not incorporated in the theories but that might be important to consider to better understand the ELA / stress response system relationship. 43. Tagung Psychologie und Gehirn | Trier 2017 3 SYMPOSIEN Brain structural alterations in newborns of mothers exposed to childhood trauma Buss, Claudia; Moog, Nora; Entringer, Sonja; SYMPOSIEN DONNERSTAG Rasmussen, Jerod; Styner, Martin; Gilmore, John; 08:30–10:00 Heim, Christine; Wadhwa, Pathik Charité Universitätsmedizin Berlin, Deutschland Stress and the brain – effects of type and "Childhood trauma (CT) confers deleterious long-term consequences and growing evidence suggests some of the timing of adversity on brain structure and effects may be transmitted across generations. We sought function to elucidate whether changes in infant brain structure were already visible shortly after birth to address the hypothesis Dennis Golm & Robert Kumsta that such intergenerational effects start in utero. King's College London, IOPPN, Vereinigtes Königreich The prospective longitudinal study was conducted in a Raum: HS 1 population-based sample of 80 mother-child dyads. Maternal CT exposure was assessed using the Childhood "Adverse experiences are a major risk factor for later life Trauma Questionnaire. Structural magnetic resonance psychopathology, especially if they occur during sensitive imaging (MRI) was employed to characterize newborn brain periods of development early in life or during adolescence. anatomy near the time of birth. Those experiences can include, but are not limited to, Maternal CT exposure was associated with lower intracra- sexual or physical abuse, socio-emotional neglect experi- nial volume in their children (F(1,72)=7.05, p=0.01), which enced by institutionalised children or serious life events. was primarily due to a global reduction in cortical gray Various mechanisms have been discussed through which matter (F(1,72)=9.32, p=0.003). The effect was independ- those risk factors lead to later-life problems such as ent of gestational age at birth and postnatal age at MRI abnormalities in brain structure and function. The aim of scan, obstetric complications, maternal socioeconomic this symposium is to explore neurobiological correlates of status, maternal depression during pregnancy and infant various risk factors experienced early in