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. 2019 Apr 17;10:404. doi: 10.3389/fphar.2019.00404

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Copyright © 2019 Torrisi, Leggio, Drago and Salomone.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The failure of the “top-down” inhibitory control exerted by the mPFC over the amygdala triggers hyperarousal and intrusion symptoms. In a normal subject (A), the mPFC exerts a homeostatic inhibitory control over the amygdala (Amy). This “top-down” brake maintains appropriate behavior patterns under stressful conditions. In PTSD patients (B) the hypoactive mPFC removes the brake over the Amy, whose hyperactivity mainly generates hyperarousal and intrusion symptoms (Fenster et al., 2018, see also text).