Highly plastic endocrine traits are thought to play a central role in allowing organisms to respond rapidly to environmental change. Yet, not all individuals display the same degree of plasticity in these traits, and the costs of this individual variation in plasticity are unknown. We studied individual differences in corticosterone levels under varying conditions to test whether there are consistent individual differences in (1) baseline corticosterone levels; (2) plasticity in the hormonal response to an ecologically relevant stressor (food restriction); and (3) whether individual differences in plasticity are related to fitness costs, as estimated by oxidative stress levels. We took 25 wild-caught house sparrows into captivity and assigned them to repeated food restricted and control treatments (60% and 110% of their daily food intake), such that each individual experienced both food restricted and control diets twice. We found significant individual variation in baseline corticosterone levels and stress responsiveness, even after controlling for changes in body mass. However, these individual differences in hormonal responsiveness were not related to measures of oxidative stress. These results have implications for how corticosterone levels may evolve in natural populations and raise questions about what we can conclude from phenotypic correlations between hormone levels and fitness measures.

Maternal effects have gained attention as a method by which mothers may alter the physiological condition and phenotype of their offspring based upon current environmental conditions. The physiological and phenotypic outcomes of glucocorticoid-mediated maternal effects have been extensively studied in a variety of vertebrates; however, the underlying mechanism is currently unclear. Here, we injected tritiated corticosterone into the yolks of freshly laid Japanese quail eggs (Coturnix japonica) and traced its movement and metabolism through the in ovo development period. We found that corticosterone was extensively conjugated throughout the egg by the end of development, and while minimal corticosterone was detected within the embryo during development, accumulation of a conjugated metabolite in the embryo started to occur on day 6 of development. Because no movement and metabolism of corticosterone occurred in infertile eggs, our findings suggest that embryos are not passive recipients of maternal steroids, but instead appear to possess extensive metabolic capabilities, which may modulate their exposure to maternal steroids.

BackgroundUnpredictable and inclement weather is increasing in strength and frequency, challenging organisms to respond adaptively. One way in which animals respond to environmental challenges is through the secretion of glucocorticoid stress hormones. These hormones mobilize energy stores and suppress non-essential physiological and behavioral processes until the challenge passes. To investigate the effects of glucocorticoids on reproductive decisions, we experimentally increased corticosterone levels (the primary glucocorticoid in birds) in free-living female tree swallows, Tachycineta bicolor, during the chick-rearing stage. Due to an unprecedented cold and wet breeding season, 90 % of the nests in our study population failed, which created a unique opportunity to test how challenging environmental conditions interact with the physiological mechanisms underlying life-history trade-offs.ResultsWe found that exogenous corticosterone influenced the regulation of parental decisions in a context-dependent manner. Control and corticosterone-treated females had similar brood failure rates under unfavorable conditions (cold and rainy weather), but corticosterone treatment hastened brood mortality under more favorable conditions. Higher female nest provisioning rates prior to implantation were associated with increased probability of brood survival for treatment and control groups. However, higher pre-treatment male provisioning rates were associated with increased survival probability in the control group, but not the corticosterone-treated group.ConclusionsThese findings reveal complex interactions between weather, female physiological state, and partner parental investment. Our results also demonstrate a causal relationship between corticosterone concentrations and individual reproductive behaviors, and point to a mechanism for why naturally disturbed populations, which experience multiple stressors, could be more susceptible and unable to respond adaptively to changing environmental conditions.

There are at least two reasons to study traits that mediate successful range expansions. First, dispersers will found new populations and thus impact the distribution and evolution of species. Second, organisms moving into new areas will influence the fate of resident communities, directly competing with or indirectly affecting residents by spreading non-native or spilling-back native parasites. The success of invaders in new areas is likely mediated by a counterbalancing of costly traits. In new areas where threats are comparatively rare, individuals that grow rapidly and breed prolifically should be at an advantage. High investment in defenses should thus be disfavored. In the present study, we compared the energetic, nutritional and collateral damage costs of an inflammatory response among Kenyan house sparrow (Passer domesticus) populations of different ages, asking whether costs were related to traits of individuals from three different capture sites. Kenya is among the world's most recent range expansions for this species, and we recently found that the expression of Toll-like receptors (TLRs), leukocyte receptors that instigate inflammatory responses when bound to microbial elements, was related to the range expansion across the country. Here, we found (contrary to our expectations) that energetic and nutritional costs of inflammation were higher, but damage costs were lower, in range-edge compared with core birds. Moreover, at the individual level, TLR-4 expression was negatively related to commodity costs (energy and a critical amino acid) of inflammation. Our data thus suggest that costs of inflammation, perhaps mediated by TLR expression, might mitigate successful range expansions.