Consistent with this hypothesis, antagonism of the CB1 receptor within the BLA increased HPA axis drive, while there was no effect of CB1 receptor antagonism within the CeA or MeA on HPA axis output. Collectively, these data suggest that AEA/CB1 receptor signaling in the BLA exerts tonic inhibition over the HPA axis. However, given that the independent effects of FAAH inhibition and CB1 receptor antagonism within the BLA on stress-induced corticosterone secretion were modest, it appears that the role of endocannabinoid signaling within the BLA is modulatory in nature.