The response to stressors in adulthood depends on the interaction between prenatal exposure to glucocorticoids and environmental context

Abstract

Maternal stress during reproduction can influence how offspring respond to stress later in life. Greater lifetime exposure to glucocorticoid hormones released during stress is linked to greater risks of behavioral disorders, disease susceptibility, and mortality. The immense variation in individual’s stress responses is explained, in part, by prenatal glucocorticoid exposure. To explore the long-term effects of embryonic glucocorticoid exposure, we injected Japanese quail (Coturnix japonica) eggs with corticosterone. We characterized the endocrine stress response in offspring and measured experienced aggression at three different ages. We found that prenatal glucocorticoid exposure affected (1) the speed at which the stress response was terminated suggesting dysregulated negative feedback, (2) baseline corticosterone levels in a manner dependent on current environmental conditions with higher levels of experienced aggression associated with higher levels of baseline corticosterone, (3) the magnitude of an acute stress response based on baseline concentrations. We finish by proposing a framework that can be used to test these findings in future work. Overall, our findings suggest that the potential adaptive nature of prenatal glucocorticoid exposure is likely dependent on environmental context and may also be tempered by the negative effects of longer exposure to glucocorticoids each time an animal faces a stressor.

Birds of a feather age together: telomere dynamics and social behavior predict life span in female Japanese quail (Coturnix japonica)

“…Higher levels of glucocorticoids inhibit aggressive behavior ( 76 , 77 ), which agrees with the results from our study. In previous work from our lab, we found that being the target of aggressive behavior increased baseline corticosterone, but only if the individuals were exposed to high levels of maternal corticosterone during embryonic development ( 21 ). This previous study suggested that maternal glucocorticoids may provide for endocrine flexibility in stressful postnatal environments, and in the light of our current work it would be interesting to know if maternal glucocorticoid exposure may also prepare offspring for a stressful environment by increasing affiliative behavior.…”

“…At the cellular level, one way that prolonged glucocorticoid exposure may have negative health effects is by increasing oxidative stress ( 14 , 18 – 21 ). Oxidative stress occurs when reactive oxygen species (ROS), many of which are byproducts of inefficient mitochondrial metabolism, damage biomolecules like DNA, lipids, and proteins ( 22 ).…”