The hypothalamus-pituitary-adrenal (HPA) axis is a key mediator of the body's response to stress. In the face of a perceived threat, hormones released from the hypothalamus result in a cascade of signaling processes with the end product being the release of the glucocorticoid cortisol, the paramount stress hormone involved in energy storage and expenditure, digestion, and immune function. Importantly, the HPA axis regulates itself by means of a negative-feedback loop. Cortisol signaling inhibits the release of hormones in the hypothalamus, down-regulating HPA axis activity and allowing the body to return to homeostasis once the perceived threat is resolved. This inhibitory signaling is mediated by glucocorticoid receptor proteins encoded by the gene NRC31 (Sapolsky, Romero, & Munck, 2000; Meaney, 2001; DeRijk et al., 2008; McEwen, 2012). Dysregulated glucocorticoid signaling disrupts HPA axis response to and recovery from a wide range of stressors, and has been implicated in child and adult manifestations of externalizing psychopathology (McBurnett et al., 1991; Hawes, Brennan, & Dadds, 2009; Lopez-Duran et al., 2009; Savitz, Lucki, & Drevets, 2009; Stadler, Poustka, & Sterzer, 2010; van Zuiden et al.,
