The mechanism by which CB1 receptor activity within the BLA regulates HPA axis activity is not known. With respect to amygdalar nuclei, the predominance of research has focused on the roles of the CeA and MeA in the neuroendocrine response to stress, while the BLA has been largely neglected (Herman et al., 2003, 2005; Dayas et al., 1999). The BLA is the integration site within the amygdala which receives afferents from cortical, hippocampal and thalamic sites encoding external sensory and visceral information (McDonald, 1992; Sah et al., 2003). Immediate early gene studies have revealed that projection neurons of the BLA are activated in response to restraint stress (Patel et al., 2005b; Reznikov et al., 2008) and lesions of the BLA dampen neuroendocrine responses to psychological stressors, such as restraint or footshock (Bhatnagar et al., 2004; Goldstein et al, 1996). Similarly, direct stimulation of the BLA can increase HPA axis activity (Szafarcyk et al., 1986; Feldman et al., 1982, 1983). Moreover, overexpression of the SK2 potassium channel in the BLA attenuates stress-induced corticosterone secretion (Mitra et al., 2009). These data suggest
