Abstract

AbstractEnvironmental challenges faced early in life can both activate and shape the development of the hypothalamic-pituitary-adrenal axis. Activation of this axis is characterized in part by elevated levels of glucocorticoids, exposure to which can have profound effects throughout an animal's life. We have demonstrated that in nestling eastern bluebirds (Sialia sialis), bouts of environmentally relevant cooling result in elevations of corticosterone (the primary avian glucocorticoid) very early in life. Nestlings repeatedly exposed to cooling also exhibit dampened corticosterone secretion later in life in response to restraint compared to control nestlings. We explored the mechanistic basis of this phenomenon. Specifically, we asked whether early-life cooling alters adrenal sensitivity to adrenocorticotropic hormone (ACTH), the primary controller of corticosterone synthesis and release. To this end, we subjected nestlings to repeated bouts of cooling (cooled nestlings) or brooding temperatures (control nestlings) early in life and, before fledging, assessed (1) the capacity of the nestlings' adrenals to produce corticosterone following ACTH injection, (2) the effect of cooling on corticosterone responses to restraint, and (3) the effect of cooling on adrenal sensitivity to ACTH. We found that both cooled and control nestlings secreted substantially higher levels of corticosterone following ACTH treatment than they did following restraint. We also confirmed that cooled nestlings had reduced corticosterone secretion in response to restraint compared to control nestlings; however, sensitivity to exogenous ACTH did not differ between temperature treatments. We hypothesize that early-life cooling alters later corticosterone secretion by affecting higher levels of the hypothalamic-pituitary-adrenal axis.

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