The low-affinity glucocorticoid receptor regulates feeding and lipid breakdown in the migratory Gambel's white-crowned sparrow Zonotrichia leucophrys gambelii.

Plasma corticosterone increases during spring migration in a variety of bird species, including the Gambel's white-crowned sparrow Zonotrichia leucophrys gambelii. Corticosterone is elevated specifically in association with migratory flight, suggesting that corticosterone may promote processes such as energy mobilization and/or migratory activity. General effects of glucocorticoids support such a prediction. Because glucocorticoids exert permissive effects on food intake, corticosterone may also participate in the regulation of migratory hyperphagia. To examine the role of corticosterone during migration, we induced Gambel's white-crowned sparrows to enter the migratory condition and compared food intake and locomotor activity between controls and birds injected with RU486--an antagonist to the low-affinity glucocorticoid receptor (GR). In addition, we investigated effects of RU486 in birds that were subjected to a short-term fast. Results indicate that RU486 did not affect locomotor activity. However, consistent with its effects in mammals, RU486 suppressed food intake. Thus, hyperphagia and migratory restlessness, the two behaviors that characterize migration, may be regulated by different mechanisms. Lastly, RU486 antagonized fasting-induced lipid mobilization, as evidenced by decreased plasma free fatty acids. Thus, data on spring migrants suggest that endogenous corticosterone levels act through the GR to support hyperphagia and that the GR promotes availability of lipid fuel substrates in association with periods of energetic demand, e.g. during migratory flight.