It should be noted, however, that we have previously found using c-fos immunohistochemistry, that CB1 receptor agonists (but not FAAH inhibitors) potentiate stress-induced neuronal activation of the CeA, but not the BLA, when administered systemically to mice (Patel et al., 2005b). It is our hypothesis that systemically administered agonists, which globally increase CB1 receptor signaling throughout the brain, promote activation of incoming excitatory afferents to the amygdala through effects in an extra-amygdalar brain region. This pattern of activation could override the local suppressive effect AEA/CB1 receptor activation within the BLA and concurrently promote activation of the CeA.
