In agreement with the model that CB1 receptor activation within the BLA limits activation of the HPA axis, local administration of the CB1 receptor agonist HU-210 into the BLA reduced the stress-induced increase in circulating levels of corticosterone. This phenomenon was mediated via a CB1 receptor dependent process (as it was prevented by co-administration of the CB1 receptor antagonist AM251), and the magnitude of this suppression was greater than what was seen following inhibition of AEA hydrolysis. In contrast, infusion of HU-210 into the CeA did not modulate the HPA axis response to restraint stress, whereas administration of HU-210 into the MeA resulted in an unexpected facilitation of stress-induced corticosterone secretion. These data demonstrate that the role of CB1 receptor signaling in HPA axis regulation is functionally dissociable among amygdalar nuclei. Given that expression analysis of the CB1 receptor reveals considerably higher densities in the BLA than in the CeA or MeA (Herkenham et al., 1991; Katona et al., 2001), it is not surprising that the most robust effects that were documented occurred through modulation of CB1 receptor signaling in
