1126 



SUBMAMMALIAN VERTEBRATES 



Hertz, 1945, 1948a, b; Haqiie, Lillie, Shaff- 

 ner and Briggs, 1949; Kline, 1955; Kline and 

 Dorfman, 1951b) or vitamin B12 deficiency 

 reduces the oviduct response, with folic acid 

 deficiency resulting in the greatest reduc- 

 tion. 



The increased response of the oviduct after 

 nicotinic acid or thiamine deficiency may be 

 the result of a decreased inactivation of es- 

 trogen by the liver, which would in effect 

 increase the levels of estrogen reaching the 

 oviduct. Nicotinic acid is part of the coen- 

 zyme involved in estrogen inactivation by 

 the liver (DeMeio, Rakoff, Cantarow and 

 Paschkis, 1948). Whether or not the de- 

 ficiencies of the other vitamins mentioned 

 causes an increased oviduct response by af- 

 fecting liver function has not been estab- 

 lished. Riboflavin according to Singher, 

 Kensler, Taylor, Rhoads and Unna ( 1944) is 

 involved in estrogen inactivation by the 

 liver; however, Kline and Dorfman (1951b) 

 could not confirm the effect of increased ovi- 

 duct response observed by Haciue, Lillie, 

 Shaffner and Briggs (1949). 



The failure of weight to increase after es- 

 trogen administration to birds in which folic 

 acid is deficient is probably the result of the 

 lack of nucleic acid synthesis. Brown (1953) 

 found that feeding of desoxy[)entose nucleic 

 acid (DNA) to folic acid-deficient chicks 

 partially restored the oviduct response to 

 estrogen. The synthesis of DNA requires in 

 turn the synthesis of considerable amounts 

 of purines. Folic acid is required for synthe- 

 sis of purines (Stokstad, 1954), whereas vi- 

 tamin B12 is implicated in the metabolism of 

 1 -carbon fragments. On the other hand, the 

 precise role that vitamin B12 plays in the 

 oviduct response to estrogen is not known. 

 Folic acid is also required for the increase 

 in size of the oviduct in response to large 

 doses of testosterone (Kline and Dorfman, 

 1951). The observation that folic acid is not 

 required for the comb response (Zarrow, 

 Koretsky and Zarrow, 1951 ) to testosterone 

 may be explained by the differences in the 

 nature of the two organs. The oviduct re- 

 sponse involves synthesis of proteins and 

 purines, whereas the comb response involves 

 the deposition of substantial amounts of 

 hyaluronic acid (Boas, 1949; Boas and Lud- 

 wig, 1950). 



B. ENDOCRIXE REGULATION OF 

 OVARIAN ACTIVITY 



1. A)iterior Pituitary 



After hypophysectomy the avian ovary 

 shows extensive atresia of the follicles and 

 regression of the medullary tissue, especially 

 of the interstitium (Hill and Parkes, 1934; 

 Schooley, Riddle and Bates, 1941; Nal- 

 bandov, 1953, 1959b, c ; Opel and Nalbandov, 

 1958). Replacement therapy with mamma- 

 lian gonadotrophins is apparently success- 

 ful in the pigeon, Columha livia (Chu and 

 You, 1946), but only partially successful in 

 chickens (Nalbandov, 1953). It is not clear 

 from the i)ublished papers whether or not 

 avian gonadotrophins are completely suc- 

 cessful. According to Opel and Nalbandov 

 (1958), some ovulations were induced (and 

 thus some follicles were maintained?) a few 

 days after hypophysectomy, but some atre- 

 sia of follicles occurred. It appears that for a 

 few hours after the withdrawal of endoge- 

 nous gonadotrophins by hypophysectomy 

 the large ovarian follicles are more suscepti- 

 ble to exogenous LH, because a dose of LH, 

 which does not cause multiple ovulations in 

 an intact laying hen, will cause their occur- 

 rence if injected into a hypophysectomized 

 hen between 6 to 12 hours after the opera- 

 tion. Within this time range, the ovary be- 

 comes more and more sensitive as the time 

 after surgery increases. In intact hens mul- 

 tiple ovulations can be obtained with ex- 

 ogenous LH provided that the hens have 

 been pretreated for about 10 days with PAIS 

 (Fraps, Riley and Olsen, 1942) or FSH 

 (Nalbandov and Card, 1946). Progressive 

 changes take place in the hypophysecto- 

 mized and the PAIS- or FSH-treated bird, 

 which also rc^sult in atresia of the follicles 

 (Fraps, Riley and Olsen, 1942; Phillips, 

 1943). It seems, thus, that atretic changes 

 in the follicle wall will predispose the follicle 

 to ovulate (Nalbandov, 1959b), but that 

 after atresia has caused breakdown of the 

 vitelline membrane, ovulation can no longer 

 be induced (van Tienhoven, 1955). Accord- 

 ing to Nalbandov (1958), ovulation is pre- 

 ceded by local ischemia of the follicular wall, 

 particularly in the region of the stigma, 

 which causes local necrosis. Whether or not 

 this necrosis is the sole local precipitating 



