eCB signaling in the BLA has also been demonstrated to play an important role in stress-induced neuroendocrine activation. In response to acute restraint stress, AEA levels are robustly decreased in the BLA, and levels of AEA are inversely correlated with plasma corticosterone levels measures after stress exposure (Hill et al., 2009). Intra-BLA infusion of a FAAH inhibitor, or a direct CB1 agonist, reduced stress-induced corticosterone release, whereas infusion of the CB1 antagonist AM251 increased corticosterone release in response to stress (Hill et al., 2009). In addition, intra-BLA infusions of Win 55212-2 blocked elevated platform-stress-induced increase in plasma corticosterone in rats (Ganon-Elazar and Akirav, 2009). These studies suggest that decreased AEA signaling in the BLA facilitates stress-induced neuroendocrine activation. With regard to long-term adaptation of neuroendocrine stress responses, Hill et al. showed that 2-AG levels in the amygdala, following repeated restraint stress, are inversely correlated with plasma corticosterone levels measured after the last restraint session (Hill et al., 2010b). Importantly, bilateral intra-BLA infusions of the CB1 antagonist, AM251, prior to the last restraint session prevented the normal habituation of the corticosterone
