Development of the chicken as a model for prenatal stress.
Exposing a pregnant mammal to stressors causes behavioral and physiological alterations in her offspring ("prenatal stress"); however, elucidation of the underlying mechanism is hindered by an inability to control maternal compounds that may affect the fetus. We designed this experiment to determine if the autonomously developing chicken embryo could be developed as a model for prenatal stress. On d 16 of incubation, eggs were treated with: 1) 60 ng corticosterone (CORT), 2) elevated incubation temperature (40.6 degrees C) for 24 h (HEAT), or 3) no treatment (Control). Chicks from all three treatments hatched at similar weights; however, HEAT chicks weighed less by 100 d of age and remained lighter until the end of the study (P < 0.05). At 8 d post-beak trimming, adrenal gland weight was not different (P > 0.20) among treatments, basal plasma corticosterone concentrations tended (P < 0.06) to be greater for CORT chicks than either the Control or HEAT chicks, and CORT chicks were heavier than HEAT chicks (P < 0.005) but not Control chicks (P > 0.20). At 11-wk, HEAT birds had heavier adrenal glands than did Control birds (P < 0.01). At 16 wk of age, Control cocks performed more (P < 0.01) pecking aggression than either HEAT or CORT cocks, whereas CORT cocks were chased more often and chased another cock less often than either HEAT or Control cocks (P < 0.01). Treatments did not alter the behavior of the hens (P > 0.10). Administration of corticosterone during incubation replicated some, but not all, of the effects seen in prenatal stress in mammals.