Effects of prenatal stress and genetics on embryonic survival and offspring growth of laying hens

Early-life exposure to stressors can shape the phenotype of the offspring resulting in changes that may affect their prehatch and posthatch development. This can be modeled indirectly through maternal exposure to stressors (natural model) or by offspring exposure to stress hormones (pharmacological model). In this study, both models were used to investigate the effects of genetic line on hatchability, late embryonic mortality, sex ratio, and body weight until 17 wk of age. To form the parent stock, fertilized eggs of 4 commercial genetic lines two brown (brown 1 and 2), two white (white 1 and 2), and a pure line White Leghorn were incubated, hatched, and housed identically in 4 flocks of 27 birds (24 females and 3 males) per strain. Each strain was equally separated into 2 groups: "maternal stress," where hens were subjected to a series of acute psychological stressors (e.g., physical restraint, transportation) for 8 D before egg collection, and "control," where hens received routine husbandry. At 3 maternal ages, fertile eggs from both treatments were collected, and additional eggs from the control group were injected with corticosterone (10 ng/ mL egg content) ("CORT"). A "vehicle" treatment was included to account for effects of egg manipulation. Each maternal age comprised a replicate over time. Eggs were incubated and hatched, and the offspring (N = 1,919) were brooded until 17 wk under identical conditions. The results show that prenatal stress interacted with strain to decrease embryonic survival and growth. Among all strains, brown 2 was consistently the most affected line in both prehatch and posthatch development. Our study shows that embryonic survival and offspring growth are mostly affected by the pharmacological model and that strain differences may increase susceptibility to prenatal stress. Moreover, it suggests that the natural stressor model may be useful for quantifying the response of the mother to stressors, whereas the pharmacological model may be useful for quantifying the response of the embryo to increased levels of corticosterone.