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→Neural Mechanism
Based on NEUROBIOLOGY OF ANXIETY: FROM NEURAL CIRCUITS TO NOVEL SOLUTIONS?<ref>[http://etkinlab.stanford.edu/Etkin%20Publications/Etkin,%20neurobio%20of%20anxiety%20from%20neural%20circuit%20to%20novel%20solution%20editorial%202012.pdf paper from 2012 Amit A., NEUROBIOLOGY OF ANXIETY: FROM NEURAL CIRCUITS TO NOVEL SOLUTIONS?,''DEPRESSION AND ANXIETY'' 29:355–358 (2012)]</ref>.
Strikingly, all three disorders (of fear) , despite differing levels of severity and generalization, resulted in '''hyperactivation of the [[amygdala ]] and insula''' in patients, a pattern also observed during fear conditioning in healthy subjects. A large body of neuroimaging work on fear conditioning and fear extinction in healthy subjects also implicates dorsal anterior cingulate and medial prefrontal ([[ACC]]/mPFC) regions in the monitoring and expression of fear responses (e.g. autonomic responses), and the ventral(or rostral) ACC/mPFC in the inhibition or extinction of these responses (10). We have shown using an emotional conflict task, that dorsal ACC/mPFC activity tracks the disruptive effects of emotional conflict, whereas ventral ACC/mPFC regulates it (11–14).
'''Emotion regulation and fear regulation may have the same circuitry''': This similarity in neural circuitry between fear condition- ing/extinction and emotional conflict regulation suggests that both may tap into the same broader emotion regulatory network in the brain (10). These findings also accord well with work in rodents, wherein prelimbic cortex (homologous to human dorsal ACC/mPFC) is involved in expression of conditioned fear, whereas the infralimbic cortex (homologous to ventral ACC/mPFC) is required for fear extinction (15).