Oxytocin reshapes fear control: intensity-dependent prefrontal dominance and whole-brain integration during naturalistic viewing
Oxytocin may reduce subjective fear responses during high-stress situations, but its clinical implications require further investigation.
Where it sits
this study against the rest of the oxytocin corpusSummary and findings
This study measured the effects of intranasal oxytocin on subjective fear in 67 healthy men during prolonged naturalistic viewing of a horror movie. The findings suggest that oxytocin reduced subjective fear after accounting for baseline ratings. Neuroimaging analyses indicated changes in brain activity associated with fear regulation.
Abstract
Anxiety and maladaptive fear remain difficult to treat, and despite initial promising findings, evidence regarding the anxiolytic and translational potential of oxytocin (OT) remains inconsistent. In a preregistered, randomized, double-blind, placebo-controlled, parallel-group pharmaco-fMRI study in 67 healthy men, we tested whether intranasal OT reduces post-exposure subjective fear during prolonged naturalistic viewing a horror movie comprising independently defined low-, medium-, and high-fear segments. OT reduced subjective fear following naturalistic threat exposure after accounting for pre-exposure baseline ratings. Neuroimaging analyses revealed that OT attenuated recruitment of the dorsolateral prefrontal cortex particularly during higher fear, and enhanced coupling of this region with the bilateral amygdala. At the large-scale network level, OT increased communication between frontoparietal/default-mode control networks and subcortical/limbic networks during high fear indicating more integrative fear regulation. A whole-brain fear neuromarker (CAFE) further confirmed intensity-dependent OT effects. Together, these findings indicate that OT modulates post-exposure fear experience and fear-related neural dynamics in ecologically valid contexts. Highlights Intranasal OT reduced post-exposure subjective fear after controlling for baseline ratings. OT modulated dlPFC activity and dlPFC-amygdala coupling under higher fear contexts. OT increased control-to-limbic/subcortical network communication selectively when fear is elvated. OT altered whole-brain fear-related neural representations in an intensity-dependent manner.
Background
Not reported in abstract.
Methods
Not reported in abstract.
Results
Not reported in abstract.
Interpretation
Not reported in abstract.
Limitations
Not reported in abstract.