Boosting oxytocin after trauma: Effects of oxytocin on fear neurocircuitry in patients with post-traumatic stress disorder

The neuropeptide oxytocin has been suggested as promising pharmacological agent to boost treatment response in post-traumatic stress disorder (PTSD). As first step to investigate the clinical potential of oxytocin in PTSD, a randomized placebo-controlled cross-over fMRI study was conducted in police officers with and without PTSD. In this PhD thesis, the effects of a single oxytocin administration on fear neurocircuitry were investigated in male and female PTSD patients.
Potential anxiolytic effects of oxytocin administration were observed in PTSD patients: oxytocin resulted in decreased subjective anxiety and nervousness, dampened amygdala activity towards emotional faces and normalized aberrant amygdala functional connectivity with prefrontal areas. Additionally, oxytocin altered neural processing of negative stimuli during distraction as emotion regulation strategy in PTSD patients in as sex-dependent manner. The effects of oxytocine were dependent on baseline neural fear regulation abilities, which were related to sex and (severity of) PTSD symptoms. Therefore, investigating the effects of oxytocin on psychotherapy, while elucidating potential contextual and inter-individual moderators, is a promising avenue for future clinical research.
Additionally, functional and structural connectivity alterations were investigated in PTSD patients: a meta-analysis and systematic review were performed on all currently available resting-state studies in PTSD and a diffusion tensor imaging (DTI) was conducted to investigate white matter integrity of major white matter tracts in PTSD. In line with the predominant neurocircuitry model of PTSD, findings suggested diminished functional and structural connectivity between the amygdala and prefrontal cortex in PTSD, possibly underlying diminished prefrontal top-down control over the fear response.