In contrast to the PFC and hippocampus, amygdalar structures appear to be positively regulated by chronic stress. Expression of CRH in the central nucleus of the amygdala (CeA) is increased under conditions of chronic stress or glucocorticoid excess (Makino et al., 1994, 1999; Shepard et al., 2000, 2003). Moreover, glucocorticoid implants in the CeA increase corticosterone responses to acute stress, suggesting a positive glucocorticoid feedback effect mediated by this region (Shepard et al., 2003). The CeA is linked to excitation of the HPA axis, mediated by inhibition of inhibitory relay neurons innervating the PVN (including the BST and dorsomedial hypothalamus, which are also implicated in inhibition by the PFC and hippocampus) (Herman et al., 2003). Thus, in addition to impairing feedback inhibition, chronic stress may permit feed-forward activation of the PVN by way of the amygdala.
