that are widely expressed in threat-transducing (i.e. fear) pathways and in systems that activate counter-regulatory activity (e.g., autonomic nervous system; Bale and Vale, 2004). Importantly, extra-hypothalamic CRH is produced largely by CRH-producing neurons in the central nucleus of the amygdala (Rosen and Schulkin, 1998). There is substantial evidence that the central nucleus of the amygdala (CeA) and bed nucleus of the stria terminalis (BNST) are key regions in organizing fear and defensive responses to psychological stressors (Davis et al., 1997; LeDoux and Phelps, 2000). We refer to this as the “threat system” and further define it as a rapid appraisal-response system due to its capacity to orchestrate rapid reactions with little cortical processing (LeDoux & Phelps, 2000). The amygdala/extended amygdala system functions to modulate cognition, behavior, and endocrine/autonomic activity through extensive afferent and efferent connections with cortical and subcortical structures (Adolphs, 2003). The amygdala is also a target of GCs. Chronic or frequent elevations in GCs are involved in remodeling of the dendritic arborization of the amygdala (Vyas et al., 2002) and in the up-regulation of CRH activity in the central nucleus (Makino et al., 1994), potentially increasing reactivity of the threat response system. In contrast, chronic or frequent elevations
