1132 



SUBMAMMALIAX VERTEBRATES 



tivity, especially during the period of full 

 reproductive activity, but before discussing 

 this phase of the subject, the experimental 

 evidence that the hormone affects ovarian 

 activity will be reviewed. 



Nalbandov (1956), in a preliminary note, 

 presented evidence that progesterone pellets 

 implanted into immature pullets hastened 

 maturation of the ovarian follicles with a 

 consequent precocious egg production. This 

 result is consistent with the data obtained 

 by Fraps (1950) with turkeys showing that 

 PMS-stimulated follicles could be main- 

 tained by progesterone injections. It also 

 agrees with the results obtained by van 

 Tienhoven (1958) suggesting that after a 

 broody period, egg production is somewhat 

 enhanced by progesterone pellet implants. 

 On the other hand, Duchaine, Driggers and 

 Warnick (1957) observed that injections of 

 6 mg. progesterone every other day delayed 

 rather than enhanced the onset of sexual 

 maturity in 16-week-old pullets. 



Broodiness of turkeys was inhibited by 

 progesterone given in a readily absorbable 

 form (van Tienhoven, 1958; Haller and 

 Cherms, 1959) , but no effect on subsequent 

 egg production was observed. It seems, 

 therefore, that the level of progesterone al- 

 ready in the blood may determine whether 

 the action of exogenous hormone will be 

 stimulating or inhibitory. This may explain 

 the difference between the results of Nal- 

 bandov (1956) and those of Duchaine, 

 Driggers and Warnick (1957). Apparently, 

 no experiments were carried out in wiiich 

 the effect of combined treatments of gonado- 

 trophins and progesterone on the inactive 

 ovary were compared with the effect of 

 single treatments. 



Large doses of progesterone, administered 

 to laying hens in paste or pellet form, inter- 

 rupt egg production (Adams, 1955, 1956; 

 Juhn and Harris, 1956; Shaffner, 1954, 1955; 

 Harris and Shaffner, 1956), presumably by 

 causing follicular atresia. These results ob- 

 tained with forms of progesterone which are 

 relatively long acting can be explained in 

 terms of the timing of the high progesterone 

 levels with respect to the ovulation cycle of 

 the chicken. Rothchild and Fraps (1949b) 

 demonstrated that progesterone injections 

 about 36 to 38 hours before expected ovula- 



tion result in atresia of the ovarian follicles. 

 Atresia can be the result of an inhibition of 

 all gonadotrophin secretion or of the release 

 of too small an amount of LH to cause ovu- 

 lation. Which of these two occurs after the 

 progesterone administration is a matter of 

 speculation. If one accepts the evidence that 

 FSH and LH are secreted as one gonado- 

 trophic complex, then the two interpreta- 

 tions are essentially the same and differ only 

 (luantitatively. Recently, van Tienhoven 

 (1959) and Nalbandov (1959a) have de- 

 fended the position that the FSH and LH 

 are released as one complex. If their idea is 

 correct, the question whether progesterone 

 causes a partial or complete inhibition of 

 gonadotrophins could be answered by deter- 

 mining the total gonadotrophic potencies of 

 the pituitaries of the progesterone-treated 

 hens. On the other hand, if FSH and LH are 

 secreted as separate entities, the two inter- 

 pretations for the atresia are qualitatively 

 different, and separate assays for FSH and 

 LH in the pituitaries of progesterone-in- 

 hibited birds should be made. In contrast to 

 the atresia which occurs when progesterone 

 is given 36 to 38 hours before ovulation, pre- 

 mature ovulations result when progesterone 

 is given 2 to 24 hours before the expected 

 ovulation (Fraps, 1955b, for review). 



Considerable evidence has accumulated 

 indicating that progesterone acts through a 

 neural mechanism to cause the release from 

 the pituitary of the gonadotrophin which in- 

 duces ovulation. This evidence can be sum- 

 marized as follows: 



1. Progesterone-induced ovulation in the 

 hen can be prevented by the simultaneous 

 or previous administration of such adrenei'- 

 gic blocking agents as SKF 501 (Zarrow 

 and Bastian, 1953), Dibenamine (van Tien- 

 hoven, Nalbandov and Norton, 1954), Di- 

 benzyline (van Tienhoven, 1955), and the 

 anticholinergic agent, atropine (Zarrow and 

 Bastian, 1953; van Tienhoven, 1955). Re- 

 cently, Moore (1958) questioned the va- 

 lidity of the argument that large amounts 

 of such agents block ovulation by blocking 

 a neural mechanism. As Everett has pointed 

 out in his chapter, "blocking" agents must 

 be given between 2:00 and 4:00 p.m. on the 

 day of the proestrum if they are to block 

 ovulation in rats. Moore (1958) adminis- 



