A recent report has demonstrated that endocannabinoid signaling within the BLA is also critical for the consolidation of aversive memories (Campolongo et al., 2009). Moreover, this research demonstrated that endocannabinoid signaling in the BLA was also required in order for corticosterone to modulate aversive memory consolidation (Campolongo et al., 2009), suggesting that glucocorticoids were capable of inducing amygdalar endocannabinoid synthesis in vivo (Hill and McEwen, 2009). As the current data indicate that stress decreases amygdalar AEA content, collectively, these studies would suggest that stress and glucocorticoids differentially affect amygdalar endocannabinoid content, per se. That is stress may decrease amygdalar endocannabinoid tone, through a glucocorticoid-independent mechanism of action, while glucocorticoids in the absence of stress may promote amygdalar endocannabinoid signaling. In a similar vein, unlike stress exposure, administration of glucocorticoid hormones can actually promote emotional flexibility and enhance fear extinction (de Quervain et al., 2009; Yang et al., 2006). Given the parallels between the effects of stress and glucocorticoids on fear extinction and amygdalar endocannabinoid signaling, the distinct possibility exists that endocannabinoid signaling is a direct mediator of these processes on adaptive emotional flexibility. Future research is required to address this question.
