Events that threaten the physical or social self, or anticipation of such events, activate physiological systems that serve defensive functions, increasing chances of survival. The body's response to threat aims to achieve allostasis, or the maintenance of stability (i.e., functioning), through activation of stress-mediating systems (McEwen, 2000). Mammals have two core stress systems: the hypothalamic-pituitary-adrenocortical (HPA) system, with its primary glucocorticoid end product (cortisol in humans and corticosterone in rodents), and the sympathetic-adrenomedullary system and accompanying norepinephrine system in the locus coeruleus. Successfully activating these systems allows adaptation to immediate and future environments, while failing to maintain stability in response to environmental threats can lead to maladaptive outcomes. How environmental conditions shape these systems is critical to understanding the development of psychopathology, particularly following early adversity.Studies with rodents have provided valuable insight into the malleability of stress-responsive systems, including strong evidence of a sensitive period, roughly equivalent to the third trimester of pregnancy and the first months of life in humans, for establishing set points for the reactivity and regulation of the HPA system (Lupien et al., 2009). Along with emerging longitudinal evidence in humans, rodent models suggest the possibility of a second time of heightened plasticity during the peripubertal period, when the HPA system can recalibrate, provided the level of physical and social threats in the environment has changed from the earlier sensitive period (Francis et al., 2002;. Similar patterns have not been found for the