Leonie Herrmann

TL;DR: This study in mice and humans presents FKBP5 as a decisive factor for the physiological stress response, shaping neuroendocrine reactivity as well as coping behavior, lending strong support to the concept emerging from human studies of FK BP5 as important factor governing gene-environment interactions relevant for the etiology of affective disorders.

TL;DR: It is demonstrated that traumatic experience in mice causes a reduction in HPC and central amygdala volume possibly due to a shrinkage of axonal protrusions and enriched housing decreased the intensity of trauma-associated contextual fear, independently of whether it was provided before or after the shock.

TL;DR: The results not only enlighten the path of NPS in the brain, but also establish a non-invasive method for NPS administration in mice, thus strongly encouraging translation into a novel therapeutic approach for pathological anxiety in humans.

TL;DR: HPA-axis reactivity endophenotypes are identified and characterized for the first time to offer an explanation for the inconsistent reports on HPA- axis function in PTSD and suggest that most likely other factors play a decisive role in determination of PTSD core symptom severity.

TL;DR: It is suggested that traumatic stress and fluoxetine interact to cause distinct alterations in the mouse PFC miRNA signature in the long-term, as well as a significant reduction in mmu-miR-1971 expression.