Modification of prenatal stress effects in rats by dexamethasone and adrenocorticotrophin.

To determine if effects of prenatal stress on offspring are mediated by the maternal pituitary-adrenocortical (PAC) system, female rats were stressed during gestation while manipulating their PAC output and the growth and behavior of their offspring examined. Specifically, females were injected with ACTH, dexamethasone (DEX), or saline (SAL) during pregnancy or were untreated (CON). Half the females in each group received daily electric shock sessions from Day 7 to Day 21 of gestation. Significantly more females in the ACTH and SAL groups delivered their litters late. Although DEX produced a significant reduction in birth and weaning weights of offspring whereas ACTH did not, both DEX and ACTH blocked the increase in birth weights produced by prenatal stress in offspring of SAL treated females. However, the significant effect of stress on mortality from birth to weaning was potentiated by ACTH and mortality was increased by either DEX or ACTH alone (compared to SAL). In addition, ACTH reversed the effect of stress on open-field activity of 86–96 day old offspring: stress reduced activity of SAL offspring but increased that of ACTH offspring. DEX itself significantly increased activity of female, but not male, offspring and ACTH significantly decreased activity of unstressed offspring of both sexes. Open-field behavior of 32–38 day offspring and active and passive avoidance conditioning of 86–96 day offspring were unaffected by prenatal drug or stress treatments. Attenuation of the maternal PAC response to stress consistently blocks the effects of prenatal stress on birth weights of offspring but can potentiate, reverse, or fail to modify the effects of stress on behavior. It thus seems unlikely that prenatal stress effects on offspring behavior are mediated by the maternal PAC system.