The role of baseline corticosterone in the regulation of avian migration

Elevated levels of plasma corticosterone have been identified during the course of spring migration in a variety of birds. However, the specific role of corticosterone in the regulation of migratory processes remains unclear. General actions of glucocorticoids include the promotion of metabolic homeostasis, and the stimulation of feeding and locomotory activity. Thus, corticosterone may participate in the regulation of hyperphagia and migratory restlessness—the two states that characterize birds in a migratory condition.; To help elucidate the migratory role of corticosterone, plasma corticosterone concentrations were determined during the stages of migratory fueling and flight in the bar-tailed godwit Limosa lapponica and the white-crowned sparrow Zonotrichia leucophrys gambelii. Because migratory fueling and flight are characterized by distinct behavior and physiology, we predicted that stage-specific differences in corticosterone would suggest the processes affected. This study found that peak corticosterone levels occurred in association with migratory flight, suggesting that corticosterone may affect energy mobilization and activity. Corticosterone may regulate migration at sub-stress baseline levels, because elevations in corticosterone did not approach maximal concentrations.; To experimentally determine the role of corticosterone during the period of migration, behavior and physiology were compared between migrants injected with RU486 and vehicle. RU486 is an antagonist to the low-affinity glucocorticoid receptor (GR). Two migratory species were investigated—the white-crowned sparrow and the red knot Calidris canutus. Consistent with its effects on mammals, RU486 treatment suppressed food intake in both investigated species. However, no effects on locomotor{09} activity were observed. Previous studies have suggested that corticosterone regulates locomotor activity through a membrane receptor. Thus, hyperphagia and migratory restlessness, the two behaviors that characterize migration, may be regulated by different mechanisms. RU486 treatment also antagonized fasting-induced lipid mobilization, as evidenced by suppressed plasma levels of free fatty acids.; In summary, data suggest that during migration, endogenous levels of corticosterone act through the GR to promote hyperphagia and lipid mobilization. Future studies will hopefully elucidate the importance of seasonal changes in GR number in the regulation of migration and will begin to address how corticosterone may interact with other hormones and neurotransmitters to regulate behavioral and physiological processes.