Characterizing the effects of early life cooling on HPA axis development in free-living songbirds


Meeting Abstract

P2-107  Saturday, Jan. 5 15:30 – 17:30  Characterizing the effects of early life cooling on HPA axis development in free-living songbirds LYNN, S.E.*; KERN, M.D.; The College of Wooster slynn@wooster.edu

Early life experiences can affect the function of the hypothalamo-pituitary-adrenal (HPA) axis of vertebrates, with potential fitness consequences. We have shown that repeated drops in body temperature during the first week of life of eastern bluebird (Sialia sialis) chicks, such as those which occur when females are away from the nest, dampen the chick HPA response to restraint prior to fledging. To explore which aspects of the HPA axis are affected by cooling, we subjected chicks to experimental cooling during the first week of life (Cooled chicks) or maintained chicks at brooding temperatures (Controls). Prior to fledging, we characterized corticosterone (CORT) secretion after (1) 60 min of restraint (to confirm the effects of cooling on HPA activity), (2) injection with adrenocorticotropic hormone (ACTH; to assess adrenal sensitivity), or (3) a dexamethasone (DEX) suppression test (to characterize negative feedback sensitivity of the HPA axis). We confirmed that repeated cooling early in life reduced CORT secretion in response to later restraint. Sensitivity to ACTH challenge did not differ between temperature treatments, but, compared to Controls, Cooled chicks exhibited impaired negative feedback sensitivity. This unexpected result does not, however, explain our consistent finding that Cooled chicks have a lower CORT response to restraint than Controls. Our data suggest that early life cooling alters the HPA axis at multiple levels. We hypothesize that cooling also alters HPA axis function at the level of the hypothalamus or anterior pituitary. Such effects are likely to be strong, with early life cooling producing an overall dampening of CORT secretion in response to novel stressors, despite impairing negative feedback of the HPA axis to glucocorticoids.

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