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 the BLA. Additionally, the fact that administration of a CB1 receptor agonist into distinct amygdalar nuclei exerted different responses on stress-induced corticosterone secretion, confirms that the effects are due to CB1 receptor activation within these restricted regions and not due to spillover of the infusion into surrounding amygdalar regions.
