Chunk #36 — Discussion — Activation of CB1 receptors within the medial or central nucleus of the amygdala exerts differential effects on stress-induced HPA axis activation
Administration of the CB1 receptor agonist HU-210 into the MeA prior to restraint potentiated the corticosterone response to stress. Similarly, systemic administration of CB1 receptor agonists can enhance stress-induced HPA axis activation (Patel et al., 2004; Jacobs et al., 1979; Hill and Gorzalka, 2006). The present data suggest that activation of CB1 receptors within the MeA could contribute to the stress-potentiating effects of systemically administered cannabinoid agonists. Given that lesion studies have indicated that the MeA is recruited by psychological stressors to activate the HPA axis (Dayas et al., 1999; Figueiredo et al., 2003; Ma and Morilak, 2005; Herman et al., 2005), the current data suggest that CB1 receptor activation within the MeA, when coupled with stressful stimuli, promotes the output neurons of this nucleus to increase the neuronal activation of the PVN. Our finding that neither AM251 nor URB597 infusions in the MeA affected the corticosterone response to stress suggests that this CB1 receptor-mediated effect is not endogenously activated by stress.
