REPRODUCTIVE EXDOCRIXOLOC.Y IX BIRDS 



1127 



factor in ovulation remains to be determined. 

 The occurrence of ovulation in vitro (Neher, 

 Olsen and Traps, 1950), provided the fol- 

 licle is not removed from the ovary until 

 about 2 hours before expected ovulation, 

 suggests that changes other than ischemia 

 also must occur. Removal of the ovary ear- 

 lier than the designated time might be ex- 

 pected to cause ischemia of the stigma as 

 soon as the blood vessels are cut; neverthe- 

 less, no ovulation occurs when this is done. 



Replacement therapy in hypophysecto- 

 mizccl chickens (Opel and Nalbanclov, 1958; 

 Nalbandov, 1959c) or the injection of gon- 

 adotrophin into intact laying hens (Traps, 

 Riley and Olsen, 1942; Phillips, 1943) does 

 not result in maintenance or formation of 

 the follicles of graded size observed in the 

 normal ovary. Rather, the effect of injected 

 hormones has been akin to an all-or-none 

 effect: either many follicles are stimulated 

 to grow to about the same size, or no stimu- 

 lation occurs (Opel and Nalbandov, 1958; 

 Nalbandov, 1959c). The mechanisms in- 

 volved in the gradation of the follicles in 

 the normal ovary awaits further elucidation. 



Gonadotrophin administration to intact 

 chickens has different effects depending on 

 the maturity of the birds. Until about 120 

 days of age, the response of the chicken 

 ovary to mammalian gonadotrophin con- 

 sists mainly of increases in estrogen and an- 

 drogen secretions and of hypertrophy of the 

 ovarian medulla. Evidence for the increase 

 m estrogen production was hypertrophy of 

 the oviduct (Domm, 1937; Domm and Van 

 Dyke, 1930; Asmundson and Wolfe, 1935; 

 Asmundson, Gunn and Klose, 1937; Lorenz, 

 1939; Nalbandov and Card, 1946 », and in- 

 creased blood lipids (Lorenz, 1939). In- 

 creased androgen secretion was indicated by 

 growth of the comb (Domm and Van Dyke, 

 1930; Domm, 1937; Asmundson, Gunn and 

 Klose, 1937; Nalbandov and Card, 1946; 

 Taber, 1948; and Das and Nalbandov, 

 1955). The hypertrophy of the medulla ac- 

 counts almost entirely for the increase in 

 ovarian weight. None of the workers who in- 

 jected mammalian gonadotrophins found 

 normal development of the follicles. This 

 lack of response of the follicles was not en- 

 tirely due to the absence of the "third gon- 

 adotrophic hormone," for even imi)lants of 



avian pituitaries (Domm, 1931) or daily in- 

 jections of chicken anterior pituitary pow- 

 der (CAP) did not result in large follicles 

 until the birds were about 100 to 110 days 

 old (Das and Nalbandov, 1955; Taber, 

 Claytor, Knight, Gambrell, Tlowers and 

 Ayers, 1958). There are, however, differ- 

 ences in the response of the immature ovary 

 to mammalian and avian gonadotrophins. 

 Taber, Claytor, Knight, Gambrell, Tlowers 

 and Ayers (1958) noted the following: (1) 

 mammalian gonadotrophins fail to induce 

 precocious follicular development, whereas 

 CAP can induce such development; (2) 

 mannnalian gonadotrophins cause medullary 

 distension and consequently increase ovar- 

 ian weight by about 400 per cent, whereas 

 CAP causes no medullary distension and 

 only a small (27 per cent) increase in ovar- 

 ian weight; (3) after 12 days of PMS treat- 

 ment the combs of immature pullets, which 

 were stimulated by the FMS, start to re- 

 gress, whereas with CAP treatment the 

 combs continue to grow, a result similar to 

 that obtained when the combs of hypophy- 

 sectomized and of estrogen-treated roosters 

 were being studied (Nalbandov, Meyer and 

 McShan, 1951). 



Both mammalian and avian gonadotroph- 

 ins increase the incidence of polyovular fol- 

 licles (Taber, 1948; Taber, Claytor, Knight, 

 Gambrell, Tlowers and Ayers, 1958) , indi- 

 cating that there is some response of the cor- 

 tex of the ovary to mammalian hormones. 

 The changes which make the ovary more re- 

 siionsive to avian gonadotrophins with in- 

 creasing age are not known. It is known that 

 the immature ovary responds to TSH by in- 

 creased respiration (Nalbandov and Nal- 

 bandov, 1949), but whether this response 

 changes with age has not been established. 



The lack of response of the follicles in the 

 immature ovary stands in striking contrast 

 to the enormous development of ovarian fol- 

 licles in the mature hen after either mam- 

 malian or avian gonadotrophin administra- 

 tion (Traps, Riley and Olsen, 1942; Phillips, 

 1943). The response, however, requires the 

 presence of the "third gonadotrophin," be- 

 cause in hypophysectomized hens mamma- 

 lian gonadotrophins fail to elicit the re- 

 sponse, whereas avian gonadotrophins can 

 elicit it at least temporarily (Nalbandov, 



