Current models of the patho-physiology of PTSD, an example of conditions that are characterized by diminished resilience on exposure to a traumatic stressor, involve abnormal fear learning and an underlying dysfunction in the neural circuitry of fear, comprising the amygdala, the hippocampus and the ventromedial PFC (vmPFC)72,73 (FIG. 3). Brain imaging studies in healthy participants have shown that acquisition of fear conditioning is centred in the amygdala74, whereas extinction of fear memory involves both the vmPFC and the amygdala; activation in these structures, as well as the thickness of the vmPFC, has been associated with extinction success74,75. A recent fmRI study examined the ability of physiological and neural fear responses to adapt flexibly to stimuli that changed from threatening to safe, and from safe to threatening76. Both the initial fear response and the subsequent flexible shift were associated with activation of a network that includes the amygdala, the striatum and the vmPFC76. In particular, the vmPFC seemed to mediate the shifting of fear to a different stimulus under stressful conditions76. Findings from a recent study suggest that emotion regulation —
