Glucocorticoid negative feedback as a potential mediator of trade-offs between reproduction and survival
© 2019 Elsevier Inc. A large increase in glucocorticoid hormones can inhibit or completely shut down breeding in wild animals. Because of its critical role in reducing glucocorticoids after exposure to stressors, hypothalamic–pituitary–adrenal (HPA) negative feedback could be an important mediator of the ecological trade-off between investing limited resources into survival/self vs. reproduction/offspring. Although assessing negative feedback in a standardized way using injections of the synthetic glucocorticoid dexamethasone is a straightforward procedure, we show that several different approaches are used to report negative feedback in the literature, and then demonstrate that this can in turn affect the statistical results and conclusions of a study. We then review six specific predictions about adaptive within- and across-species patterns in glucocorticoids based on the relative costs and benefits of maintaining or abandoning breeding attempts when animals are faced with prolonged strong stressors, and examine evidence for these predictions in the context of HPA negative feedback. Thus far, evidence supporting these predictions for negative feedback is mixed, with the strongest evidence supporting a link between poor body condition and weak negative feedback in breeding animals. However, more research is necessary to assess the importance of changes in HPA negative feedback, especially in reptile, fish, and amphibian species. Furthermore, future research would benefit from reporting negative feedback ability in a standardized way, or at least making raw data available for the computation of alternate measures, to more easily compare studies in this growing area of research.
Publication Source (Journal or Book title)
General and Comparative Endocrinology
Lattin, C., & Kelly, T. (2020). Glucocorticoid negative feedback as a potential mediator of trade-offs between reproduction and survival. General and Comparative Endocrinology, 286 https://doi.org/10.1016/j.ygcen.2019.113301