Early-life stress has persistent effects on amygdala function and development in mice and humans.

Relatively little is known about neurobiological changes attributable to early-life stressors (e.g., orphanage rearing), even though they have been associated with a heightened risk for later psychopathology. Human neuroimaging and animal studies provide complementary insights into the neural basis of problem behaviors following stress, but too often are limited by dissimilar experimental designs. The current mouse study manipulates the type and timing of a stressor to parallel the early-life stress experience of orphanage rearing, controlling for genetic and environmental confounds inherent in human studies. The results provide evidence of both early and persistent alterations in amygdala circuitry and function following early-life stress. These effects are not reversed when the stressor is removed nor diminished with the development of prefrontal regulation regions. These neural and behavioral findings are similar to our human findings in children adopted from orphanages abroad in that even following removal from the orphanage, the ability to suppress attention toward potentially threatening information in favor of goal-directed behavior was diminished relative to never-institutionalized children. Together, these findings highlight how early-life stress can lead to altered brain circuitry and emotion dysregulation that may increase the risk for psychopathology.