The overarching goal of our research is to understand the neurocircuitry that confers risk for psychopathology following traumatic event exposure. Existing neurocircuitry models of PTSD and trauma exposure mainly emphasize hyperactivation of the amygdala and dorsal anterior cingulate cortex to threat and hypoactivation of the medial and lateral PFC during fear inhibition and emotion regulation. While a large body of data supports these models, the goal of our research is to refine and expand these models to encompass important observations that are not well explained by these models.