ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2026
Traumatic stress recruits an excitatory orbitofrontal-amygdala pathway to drive maladaptive aggression.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- NMDA receptor-dependent structural plasticity links early life stress to persistent aggression.Neurobiology of stress · 2026Review
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Abstract
Traumatic stress is a reliable predictor of heightened aggression, yet the mechanisms linking stress exposure to aggression remain poorly understood. We previously found that traumatic stress activates the posterior ventral segment of the medial amygdala (MeApv) to drive persistent increases in aggressive behavior. However, why traumatic stress would engage an aggression-promoting pathway is unclear. To address this, we mapped the inputs to the MeApv and identified a population of excitatory, but not inhibitory, neurons in Layer 5 of the medial orbitofrontal cortex (mOFC). The OFC is classically viewed as an inhibitory brake on amygdala-driven impulses, yet emerging evidence suggests it can also facilitate context-dependent emotional responses. Notably, traumatic stress is known to disrupt OFC function and its connectivity with the amygdala, implicating this circuit in pathological aggression. Using fiber photometry, we found that traumatic stress selectively activates these MeApv-projecting excitatory mOFC (mOFC
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