Chronic Stress Intensity Does not Affect Corticosterone or DNA Damage in Adult and Juvenile House Sparrows

One unanswered question in the field of stress physiology is how the pathology associated with chronic stress arises, such as increased baseline corticosterone, blunted stress‐induced corticosterone, and increased levels of DNA damage. If the intensity of the stressor plays a role, we would expect high stress animals to develop pathologies such as these sooner or that is more severe than an animal experiencing less‐intense chronic stress. To test this, we modified an applied chronic stress protocol in both adult and juvenile house sparrows ( Passer domesticus ) and monitored a physiological mediator, corticosterone, and an endpoint, DNA damage, of the stress response. We found that neither DNA damage nor corticosterone was sensitive to the intensity of chronic stress in both ages of birds. The high‐stress adult birds had higher stress‐induced corticosterone 6 weeks after the chronic stress period ended, potentially indicating that they were prepared for future stressors, while also avoiding pathology. High levels of corticosterone after ~ 3 weeks of an acclimation period and throughout the duration of this study indicate that the birds in this study may not have fully acclimated to captivity, potentially confounding the effects of a graded chronic stress protocol. Taken together with other data from this larger project, we show that not all physiological systems are affected by chronic stress equally and that some physiological changes may be caused by pathways other than the hypothalamic‐pituitary‐adrenal axis.