Administration of hydrocortisone to the newborn rat delays the onset of the circadian rhythm by three days and the onset of the adrenocortical response to ether by two weeks (to 25 days). The time course response to ether in adrenal corticoids is sluggish and circulating corticosterone tends to be lower. However, if laparotomy is added to the ether stress, a small but significant response occurs at 20 days. At 15 days, 0.1 U ACTH/100 gm body weight in dexamethasone-blocked rats produces a diminished response at 60 minutes in hydrocortisone-treated animals compared to controls, suggesting that adrenal exhaustion may occur. Administration of varying doses of ACTH at this age reveals threshold differences in adrenal responsiveness. Subcutaneous administration of 2.5 microgram dexamethasone phosphate/ 100 gm body weight blocks the adrenocortical response to ether in hydrocortisone-treated rats only, indicating that feedback sensitivity is enhanced. Biogenic amine levels in the medical hypothalamus of 30-day-old rats also are affected. Both norepinephrine and serotonin levels are significantly elevated but dopamine levels remain unchanged. Immunological consequences of neonatal hydrocortisone treatment include decreased levels of serum globulins and IgG up to 30 days of age. This defect results from impaired endogenous production of immunoglobulins. BIBLIOGRAPHIC REFERENCES: Ulrich, R., Yuwiler, A., Geller, E., and Archer, C., "Neonatal Hydrocortisone Treatment: Effects on Adrenocortical Response to Stress and ACTH and the Central Threshold to Dexamethasone Treatment", Endocrine Society Meeting Chicago, 111. 1977. Ulrich, R., Levy, L., Kasson, B., Harwick, H.J., and Brammer, G., "Developmental Changes of Immunoglobulins in Rats Treated Neonatally with Hydrocortisone", Proc. Soc. Exper. Biol. Med. 154:107, 1977.