Blocking testosterone action indirectly increases migratory restlessness during fall migration


Meeting Abstract

P1.217  Friday, Jan. 4  Blocking testosterone action indirectly increases migratory restlessness during fall migration NEMETH, Z.*; RAMENOFSKY, M.; University of California, Davis znemeth05@gmail.com

Unlike vernal migration, the role of testosterone in initiating and organizing fall migration is unknown. Although gonads are regressed and plasma levels of androgen are low at the outset of fall migration, nongonadal (adrenal or brain) testosterone may direct the physiological processes that facilitate the development of migratory behavior. We tested this hypothesis in gonadectomized male White-crowned Sparrows (Zonotrichia leucophrys gambelii) by blocking the action of testosterone in birds completing post-breeding molt just prior to the initiation of fall migration. We monitored the development of molt, premigratory fattening and flight muscle hypertrophy as well as levels of plasma androgen (T and DHT) and estradiol (E2) and migratory restlessness (Zugunruhe) and daytime activity throughout the course of a seven-week period. We compared these parameters across three groups of birds: (i) castrates implanted with Fadrozole (aromatase inhibitor) and Flutamide (androgen receptor blocker), (ii) castrates with blank implants, and (iii) sham operated birds. All three groups completed molt, fattened and developed migratory behavior. They only differed in plasma T levels (Fad/Flut birds being lower than the other two groups) but this difference was present even before the implants were introduced. Interestingly, once the implants were removed, the Fad/Flut group significantly increased migratory restlessness over the other two groups, which also showed activity but to a lesser extent. Our results suggest that (a) gonadal T is not necessary for the development of fall migration; (b) the reduction or clearance of sources of T may be required to allow migratory restlessness to develop fully. Taken together our results indicate that migratory restlessness seems to be controlled by different pathways than either premigratory fattening or muscle hypertrophy during the fall stage.

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