and that removal of this AEA tone in response to stress may permit activation of the HPA axis. In this sense, AEA signaling may function more as a “gatekeeper” (Patel et al., 2004). Interestingly, while the locus of action for CB1 receptor antagonists to increase HPA axis activation appears to be within the PVN proper (Evanson et al., 2007), the HPA axis limiting effects of AEA appear to be due to an upstream site of action, in particular the basolateral amygdala (Hill et al., 2009c).
