The results of this study demonstrate that exposure of rats to a psychological stressor evokes an increase in FAAH-mediated hydrolysis of AEA within the amygdala, which results in a suppression of AEA/CB1 receptor signaling within the BLA. This reduction in AEA/CB1 receptor signaling within the BLA determines the magnitude of the corticosterone response during the stress-induced activation of the HPA axis. Based upon these and other findings, we propose that AEA/CB1 receptor signaling in the rat amygdala is tonically active, and that it serves as a functional gatekeeper of HPA axis activation. Thus, following exposure to stress, FAAH activity increases, which results in a drop in AEA tone that promotes neuronal activation within the BLA and increases activation of the HPA axis.
