REPRODUCTIVE ENDOCRINOLOGY IN BIRDS 



1121 



one acts synergistically with estrogen to 

 stimulate ovidiical development and secre- 

 tory activity (discussed under oviduct de- 

 velopment), and it may play a role in 

 regulating incubation behavior in the ring 

 dove {Streptopelia risoria) (Lehrman, 1958, 

 and his chapter in this book) . Progesterone, 

 in doses which also cause ovarian atresia, 

 causes molting of chickens and seems to 

 stimulate the feather papilla (Shaffner, 

 1954; Juhn and Harris, 1956, 1958). Juhn 

 and Harris (1955) defeathered birds, then 

 gave progesterone intradermally. No stimu- 

 lating effect of progesterone was observed, 

 although thyroxine treatment under similar 

 conditions was effective in stimulating the 

 feather papilla. Juhn and Harris (1955) 

 used the structure of the new feathers as 

 an ''internal assay" to detect possible stimu- 

 lation of the thyroid by the injected pro- 

 gesterone. No evidence of thyroid stimula- 

 tion was found and the hypothesis that 

 progesterone causes molt by stimulating the 

 thyroid was rejected. Himeno and Tanabe 

 (1957) arrived at a similar conclusion after 

 determination of thyroid activity with I'^^. 

 These authors suggested that the molt is 

 precipitated when the ovary becomes atretic 

 under the influence of progesterone, the con- 

 sequent reduction in circulating estrogens 

 would then allow the feather follicles to 

 become active. In addition, progesterone 

 would stimulate the feather papillae to form 

 new feathers. This hypothesis does not ac- 

 count for the fact that testosterone causes 

 cessation of laying (and thus atresia?) but 

 does not induce molting, nor does it account 

 for the precipitation of molting after preg- 

 nant mare's serum (PMS) or FSH injections 

 (Juhn and Harris, 1956) which cause atresia 

 but do not reduce estrogen secretion (Bates, 

 Lahr and Riddle, 1935) . The endocrine regu- 

 lation of molting may well be different de- 

 pending on the species. Harris and Shaffner 

 (1956) noted that progesterone fails to in- 

 duce molting in pigeons whereas similar 

 doses induce molting in chickens. Kobaj^a- 

 shi (1958) subsequently investigated the 

 effect of 17 a-oxyprogesterone-7-caproate 

 (PC) on molting of 19 avian species. He 

 found that birds which breed all year can 

 be induced to molt by PC injections, but in 

 seasonal breeders the molt fails to occur. In 



birds of the former type complete thyroid- 

 ectomy prevented the molt response to PC, 

 but gonadectomy had no effect. Kobayashi 

 proposed that the following mechanisms 

 miij;lit ])v involved in the PC-induced molt: 

 (1) inn-eased sensitivity of the feather pa- 

 pillae to thyroid hormone, which can induce 

 molt alone; (2) a synergistic action between 

 PC and thyroid hormone; (3) a combination 

 of 1 and 2. In view of the results of Juhn 

 and Harris (1958) implicating prolactin as 

 a liormone involved in molting, it seems 

 that factorial experiments with hypophy- 

 sectomized-gonadectomized birds should be 

 carried out as a means of establishing the 

 relationships between prolactin, progester- 

 one, thyroid hormone, and estrogen on molt- 

 ing. An excellent review on the endocrine 

 factors involved in molting has been pub- 

 lished by Assenmacher (1958). 



4. Huptured follicle hormone? Rothchild 

 and Fraps (1944a, b) noted that removal of 

 the recently ruptured follicle caused re- 

 tention of the egg in the oviduct from 9 

 hours to 3 days longer than normal. Re- 

 moval of the largest mature follicle caused 

 only a slight delay in oviposition, but when 

 both the recently ruptured and the largest 

 follicle were removed the egg was retained 

 for from 1 to 7 days. Subsequent investiga- 

 tions by Conner and Fraps (1954) demon- 

 strated a rather curious quantitative rela- 

 tionship between the ruptured follicle and 

 oviposition. When half of the ruptured fol- 

 licle is removed some birds show no effect, 

 others retain the egg, and a small number 

 lay the eggs prematurely. The smaller the 

 portion removed, the greater the incidence 

 of premature ovipositions. The time of re- 

 moval, apparently, also played a part, for a 

 maximal incidence of premature oviposi- 

 tions occurred when the operation was per- 

 formed about 9 hours after ovulation. 

 Although the endocrine function of the rup- 

 tured follicle has not been demonstrated by 

 replacement therapy, the evidence strongly 

 suggests that the recently ruptured follicle 

 has a rather short-lived endocrine activity. 

 The short duration of its function is indi- 

 cated by its rapid degeneration and by the 

 lack of effect when the next to last ruptured 

 follicle is removed (Rothchild and Fraps, 

 1944a). 



