Several lines of evidence have shown that traumatic events during the early postnatal period precipitate long-lasting alterations in the functional properties underlying emotional expression that are attributable to the pathophysiology of stress-related disorders. In this chapter, we summarize our recent work elucidating whether early postnatal stress alters the neural circuits underlying emotional regulation. Rats exposed to footshock stress (FS) during the second (2W) or the third (3W) postnatal week were subjected to unconditioned and conditioned stresses at the postadolescent period (10-12 weeks). No differences in locomotor activity or hippocampal synaptic changes were observed between the FS-groups and non-FS controls during exposure to open field stress. Fear-related freezing behavior during exposure to contextual fear conditioning (CFC) was markedly attenuated in the 2W-FS group, presumably due to disturbance of the retention for fear memory, an effect that was attributable to synaptic changes in the hippocampal CA1 field. The 3W-FS group exhibited attenuation of the decreases in freezing behavior induced by CFC extinction trials. The deficits in extinction was abolished by repeated treatment with the partial N-methyl-d-aspartate receptor agonist d-cycloserine, suggesting that aversive stress exposure during the third postnatal week impaired extinction of context-dependent fear memory. Taken together, the altered behavior observed in adulthood is likely the result of neurodevelopmental perturbations elicited by early life stress. Thus, a "critical period" exists for neural circuits involved in emotional expression that may contribute to lifelong susceptibility to stress.