In adulthood, the hypothalamo-pituitary-adrenal axis is controlled by both corticotropin releasing hormone (CRF) and arginine vasopressin (AVP). In neonates, however, CRF secretion is very low whereas AVP secretion is fully functional. This suggests that the role of AVP is more pronounced in young than in adult rats. We investigated the role of AVP by studying stress responses in 5, 10 and 20-day-old AVP-deficient Brattleboro rats. Two different stressors were applied: 24h maternal separation and Hypnorm injections. In heterozygous controls (that do express AVP), both stressors increased plasma adrenocorticotropin (ACTH) and corticosterone. The ACTH stress response disappeared in AVP-deficient rats demonstrating that during perinatal period the secretion of this hormone is controlled by AVP. Surprisingly, corticosterone responses remained intact in AVP-deficient rats. Similar findings were obtained after 1, 4, 12 and 24 hour-long maternal separations. Thus, preserved corticosterone stress responses were not explained by changes in the timing of ACTH secretion. In vitro experiments suggested that the dissociation of ACTH and corticosterone stress responses can only be partly explained by higher ACTH responsiveness of the adrenal cortex in AVP-deficient rats. Taken together, our results show that in neonatal periods AVP is crucial for the expression of ACTH stress responses, but neither AVP nor ACTH is necessary for the induction of corticosterone stress responses. Discrepant ACTH and corticosterone stress responses may reflect compensatory mechanisms activated by AVP deficiency but disparate findings suggest that they rather depict a neonate-specific mechanism of HPA-axis control.