Throughout life physiological systems strive to maintain homeostasis and these systems are susceptible to exposure to maternal or environmental perturbations, particularly during embryonic development. In some cases, these perturbations may influence genetic and physiological processes that permanently alter the functioning of these physiological systems; a process known as developmental programming. In recent years, the neuroimmune system has garnered attention for its fundamental interactions with key hormonal systems, such as the hypothalamic pituitary adrenal (HPA) axis. The ultimate product of this axis, the glucocorticoid hormones, play a key role in modulating immune responses within the periphery and the CNS as part of the physiological stress response. It is well-established that elevated glucocorticoids induced by developmental stress exert profound short and long-term physiological effects, yet there is relatively little information of how these effects are manifested within the neuroimmune system. Pre and post-natal periods are prime candidates for manipulation in order to uncover the physiological mechanisms that underlie glucocorticoid programming of neuroimmune responses. Understanding the potential programming role of glucocorticoids may be key in uncovering vulnerable windows of CNS susceptibility to stressful experiences during embryonic development and improve our use of glucocorticoids as therapeutics in the treatment of neurodegenerative diseases.
The responsiveness of the avian stress system declines with age. A recently published study of European starlings (Sturnus vulgaris) found that a marker of biological age predicted stress responsiveness even in individuals of the same chronological age.Specifically, birds that had experienced greater developmental telomere attrition showed a lower peak corticosterone response to an acute stressor, and more rapid recovery of corticosterone levels towards baseline. Here, we performed a follow-up study using the same capture-restraint-handling stressor in a separate cohort of 27 starlings. Unlike the original study, we measured the response at two different age points (4 and 18 months).We did not replicate the associations with developmental telomere attrition observed in the previous study at either age point. However, a meta-analysis of the present results combined with those of the earlier study still lent some support to the conclusions of the earlier paper. Estimates of familial influence on stress responsiveness differed across the two age points. We found little evidence of individual consistency in stress responsiveness between 4 and 18 months. Peak corticosterone was significantly lower at the second age point than the first, though interpretation of this as age-related decline is problematic due to the samples having been analysed at different times. found that a marker of biological age predicted stress responsiveness even in 21 individuals of the same chronological age. Specifically, birds that had experienced greater developmental 22 telomere attrition showed a lower peak corticosterone response to an acute stressor, and more rapid 23 recovery of corticosterone levels towards baseline. Here, we performed a follow-up study using the same 24 capture-restraint-handling stressor in a separate cohort of 27 starlings. Unlike the original study, we 25 measured the response at two different age points (4 and 18 months). We did not replicate the associations 26 with developmental telomere attrition observed in the previous study at either age point. However, a 27 meta-analysis of the present results combined with those of the earlier study still lent some support to the 28 conclusions of the earlier paper. Estimates of familial influence on stress responsiveness differed across 29 the two age points. We found little evidence of individual consistency in stress responsiveness between 4 30 and 18 months. Peak corticosterone was significantly lower at the second age point than the first, though 31 interpretation of this as age-related decline is problematic due to the samples having been analysed at 32 different times. , 2015). Biological age is by definition a better predictor of future lifespan than 45 chronological age is. Hence, we should expect markers of individual biological age to explain variation in 46 stress responsiveness that cannot be explained by chronological age alone. A possible reason that early-47 life conditions have often been observed to influence the functioning of the adult stress respon...
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