function are mimicked by administration of chronic corticosterone to animals (Hill et al., 2008a; Bowles et al., 2011) and blocked by antagonizing glucocorticoid receptors (Gorzalka and Hill, 2011). Thus, stress appears to modulate eCB signaling via the Hypothalamic-Pituitary-Adrenal-Axis (HPA), which is responsible for regulating glucocorticoid levels (stress hormones) in response to environmental stressors.
