The data presented here show for the first time that pharmacological blockade of KOR in the CeA with nor-BNI decreases pain-like and averse-affective behaviors by enhancing or restoring synaptic inhibition of CeA-CRF neurons in an FPS model, indicating a functional correlation between pain behaviors and KOR signaling in the amygdala in a functional pain syndrome (FPS) condition. The gene discussed is CRH; the disease is Fontaine progeroid syndrome.