Recent studies have focused on the behavioral and neurobiological sequella of exposure toearly adverse events. We hypothesize that early adverse experiences result in an increasedsensitivity to the effects of stress later in life and render an individual vulnerable to stress-relatedpsychiatric disorders. This vulnerability may be mediated by persistent changes incorticotropin-releasing-factor (CRF)-containing neurons, thehypothalamic–pituitary–adrenal axis, and the sympathetic nervous system. Wetherefore present an overview of the CRF system and its role as a mediator in the development ofthe stress response, major depression, and posttraumatic stress disorder. The literature pertainingto behavioral and neurobiological alterations associated with exposure to early adverse life eventsin rodents, nonhuman primates, and humans is reviewed. We focus on animal models thatprecipitate depressive and anxiety symptoms while producing neuroendocrine alterations thatmimic those seen in adults with those disorders. The literature integrating neurobiological andbehavioral consequences of early life stress is also reviewed, focusing primarily on infants bornto mothers with depression and on infants who were abused or neglected.