Abstract
Early embryonic exposure to maternal glucocorticoids can broadly impact physiology and behaviour across phylogenetically diverse taxa. The transfer of maternal glucocorticoids to offspring may be an inevitable cost associated with poor environmental conditions, or serve as a maternal effect that alters offspring phenotype in preparation for a stressful environment. Regardless, maternal glucocorticoids are likely to have both costs and benefits that are paid and collected over different developmental time periods. We manipulated yolk corticosterone (cort) in domestic chickens (Gallus domesticus) to examine the potential impacts of embryonic exposure to maternal stress on the juvenile stress response and cellular ageing. Here, we report that juveniles exposed to experimentally increased cort in ovo had a protracted decline in cort during the recovery phase of the stress response. All birds, regardless of treatment group, shifted to oxidative stress during an acute stress response. In addition, embryonic exposure to cort resulted in higher levels of reactive oxygen metabolites and an over-representation of short telomeres compared with the control birds. In many species, individuals with higher levels of oxidative stress and shorter telomeres have the poorest survival prospects. Given this, long-term costs of glucocorticoid-induced phenotypes may include accelerated ageing and increased mortality.
Highlights
Vertebrates respond to stress by activating a suite of integrated physiological response mechanisms termed a stress response, of which a key component is the hypothalamicpituitary-adrenal (HPA) axis
We examined the effect of prenatal exposure to elevated yolk cort on the function of the HPA axis and on oxidative stress post-hatch
Embryonic exposure to cort increased the duration of the acute stress response and the proportion of short telomeres in the high-cort group, while baseline reactive oxygen metabolites (ROMs) levels were increased in both cort treatment groups
Summary
Vertebrates respond to stress by activating a suite of integrated physiological response mechanisms termed a stress response, of which a key component is the hypothalamicpituitary-adrenal (HPA) axis. These processes are probably best understood in the rat model, where maternal cort in developing rats reduce the number of glucocorticoid type I and II receptors in the hippocampus [31] This reduction results in impaired negative feedback control of cort secretion, which often produces higher baseline levels and a prolonged duration of the stress response [7]. (e) Statistics For growth, plasma cort and oxidative stress analyses, we tested the effects of sex, treatment and their interaction on our response variables. Our sample size of seven individuals per treatment limited degrees of freedom and made it necessary to limit analysis to 12 of the 40 TRF intervals as dependent variables (1–5 kb, and every 5 kb thereafter) These intervals were chosen to enable us to compare treatments across the entire TRF distributions, while providing more information at the low MW regions where short telomeres lead to telomere dysfunction. We report means + standard error of the mean (s.e.m.)
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