Team (from left to right): Mitjan Morr, Jule Daniels, Dirk Scheele, Jeanine Noell, Daphne Sassin

Severe traumatic experiences such as falling victim to assault, torture, or rape have deleterious effects. Clinical manifestations include intrusions, avoidance behavior, and hyperarousal, which are associated, at a circuit level, with hyperfunction of the amygdala and hypofunction of prefrontal cortex (PFC) subregions. In up to 50 % of the cases, resilience is not sufficient and trauma-exposed individuals develop posttraumatic stress disorder (PTSD). Social support has stress-protective effects and is mediated by the hypothalamic peptide oxytocin (OT). This peptide hormone exerts anxiolytic effects by inhibiting the amygdala and strengthening amygdala-PFC interactions. Recent clinical trials provide preliminary evidence that post-trauma administration of OXT could be effective as a preventive intervention for PTSD in a subsample of individuals exhibiting early PTSD symptoms prior to the onset of the disorder. However, the underlying neurobiological mechanisms are unclear. 

Therefore, the rationale of the present project is to expose a pre-stratified sample of vulnerable, lonely healthy participants to experimental trauma in order to explore the circuit mechanisms by which social support and OXT influence, and interfere with, traumatic experience. In a first study, we will employ functional magnetic resonance imaging (fMRI) in order to elucidate the long-term effects of intranasal OXT on (i) trauma-induced intrusions, (ii) amygdala responses during an emotional face matching task, and (iii) amygdala-PFC resting state connectivity. In a second study based upon the same paradigms, we will employ an fMRI-guided excitatory theta-burst transcranial magnetic stimulation (TMS) protocol in order to explore if the effects of social support can be mimicked by enhancing top-down PFC control over amygdala responses.

This project is funded by the Else-Kröner Fresenius Stiftung (EKFS).