Irina A. Ionescu

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: 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: This study demonstrates for the first time that a loss of hippocampal synaptic proteins is associated with a PTSD-like syndrome in mice, and demonstrates that treatment with the serotonin reuptake inhibitor (SSRI) fluoxetine is able to counteract both the PTSD- like syndrome and the posttraumatic synaptic protein loss.

TL;DR: It is found that Fkbp5 deletion, which was previously demonstrated to improve stress-coping behavior in mice, prevents the stress-induced decline in prefrontal cortical (pc), but not in hippocampal synapsin expression, and gene expression levels of SYN1, SYN2 and FKBP5 correlated positively with a more active mouse stress coping behavior.