Regulation of stress reactivity within an ecological context
Over the last few years, I have used the tools from my postdoctoral work to examine the regulation of stress reactivity in two separate studies. The first study was designed to examine the plasticity of the stress response among three subspecies of the white-crowned sparrow. The three subspecies have different distributions that are likely to affect the evolutionary pressures shaping the stress response. In particular, these sparrows breed at different elevations and latitudes and thus have breeding seasons that differ markedly in length. We hypothesized that in populations where birds raise only one or rarely two broods in a season, the fitness costs of abandoning a nest is substantially larger than in closely related populations that raise up to three broods per season. Thus, individuals with short breeding seasons should be less responsive to stressors, and therefore less likely to abandon their young. I measured glucocorticoid secretion (both baseline and stress induced), plasma binding globulin (to estimate tissue availability of circulating glucocorticoids), as well as neural and hepatic intracellular receptor levels to gain an integrated perspective of the stress-responsivity of each subspecies. Contrary to our hypothesis, basal and stress-induced glucocorticoid levels were similar in each sub-species. However, corticosteroid binding globulins differed—leading to a direct relationship between stress-induced free (unbound) CORT levels and length of breeding season. There were also population-specific differences in intracellular receptors in both liver and brain tissue.
The second study also measured several components of the stress response pathway, but examined the regulation of these components in one population of house sparrows over the annual cycle. Using a resident population of house sparrows, I measured plasma glucocorticoid and binding globulin levels, and neural intracellular and membrane corticosteroid receptors in breeding, molting, and wintering birds, with exciting results. As previously demonstrated by Wingfield and colleagues in multiple species, there is a robust seasonal rhythm to both baseline and stress-induced glucocorticoid secretion in house sparrows. However, there is a similar seasonal rhythm to corticosterone binding globulin levels, so that estimated free (unbound and available to tissues) levels are the same year-round. Seasonal patterns of total glucocorticoids and corticosteroid binding globulins are similar in white-crowned sparrows, redpolls, long-spurs, and snow buntings (studies by Romero and Wingfield where free levels were not calculated), indicating that this phenomenon may be widespread. If true, we may need approach seasonal changes in total hormones not as a mechanism to deliver more hormone to tissues, but to change the reservoir of hormones in the blood. In the seasonal house sparrow study, there is also seasonal regulation of both membrane and intracellular receptor levels, but the two receptor systems are independently regulated, with membrane receptors at their lowest levels during breeding, and intracellular receptors at their lowest levels during winter.
Taken together, these two studies indicate that contrary to current thinking, measurements of total hormone alone may not correctly evaluate the biological output of the stress response; that consideration of downstream components, especially binding globulins, may offer greater insight into the whole organism response to changing environmental conditions.