We have previously suggested a possible role of increased maternal corticosterone (CORT) secretion in mediating the endocrine effects of prenatal alcohol administration. We tested this hypothesis by adrenalectomizing pregnant rats and exposing them to high levels of CORT that mimicked those previously measured in intact dams exposed to alcohol. CORT (28 mg/day) or placebo pellets were placed subcutaneously in adrenalectomized (ADX) dams during Days 8-14 of gestation. At 21 days of age, the offspring were either decapitated under nonstressed conditions or exposed to mild, inescapable electroshocks (1.5 mA; 1 s duration; 2.5/min) over a 10-min period and then sacrificed. Plasma ACTH and CORT levels were measured by radioimmunoassay. There were no measurable differences between basal or stress-induced ACTH secretion of pups born to ADXCORT or ADX-placebo dams. In contrast, the offspring of ADX-CORT dams demonstrated significantly (P 0.01; P 0.05) lower CORT secretion when exposed to the shocks despite unaltered basal levels. Measurement of CRF expression by in situ hybridization methodology indicated no difference between CRF biosynthesis of both groups of pups. These results do not support the hypothesis that the increased stress-induced ACTH release of rats born to intact dams exposed to alcohol is primarily mediated by increased maternal corticosterone levels.