Endocrine Abstracts

Exposure to stressful events during development is known to have significant effects on a range of phenotypic traits in later life. Several mammalian studies have linked early post-natal stress to later changes in the hypothalamic pituitary adrenal (HPA) axis, underlying the physiological response to stress. However, the physiological link (lactational hormonal transfer) between mother and offspring during post-natal development limits our ability to determine the direct effects of glucocorticoid exposure in post-natal life on subsequent stress responses, as the dosage experienced by the offspring may vary with time and feeding regime. Here we present a novel model using an avian species, the zebra finch (Taeniopygia guttata), in which maternal hormonal transfer during post-natal development is absent. Post-natal exposure of chicks to the glucocorticoid hormone corticosterone (CORT) was manipulated for a 16-day period up until nutritional independence (28 days) and the long term effects on the physiological response to stress determined. CORT doses were scaled to mimic the physiological response of juvenile birds to a capture-handling-restraint protocol. There were no effects of developmental CORT treatment on baseline CORT concentrations at 60 days (F_1,26=0.51, P=0.48). However, CORT-fed birds showed exaggerated (F_1,26=8.1, P=0.008) and prolonged responses (F_1,20=5.67, P=0.03) to acute stress at 60 days of age. There were no effects of growth rates or sex on stress responses in later life. Our results clearly demonstrate that post-natal stress has significant long-term effects on the physiological stress response in birds and provides a potential mechanism underlying long-term behavioural responses to developmental conditions. This study represents the first direct evidence for post-natal glucocorticoid programming of the hormonal phenotype using this novel model for post-natal stress. This model therefore provides an important tool with which to investigate the role of glucocorticoids in shaping adult phenotypes.