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