174 John Hammond, Jr. 



DISCUSSION 



Both in immaturity and with poor nutritive conditions it seems that there 

 may be impaired follicle growth and ovulation in response to PMS. It 

 also seems that pituitary extracts are then more cftective than is PMS. If 

 this is because PMS requires the synergism of endogenous LH, one 

 might suppose that immaturity and low plane of nutrition depress LH 

 secretion. 



It is an accepted belief with sheep that "flushing" — raising the plane of 

 nutrition shortly before mating — increases the ovulation rate. Wisconsin 

 workers (32) would revise this, and say that flushing raises the rate to normal. 

 However that may be, Wallace (76) found that both PMS treatment and 

 flushing raise the ovulation rate, and that both also shorten the cycle length. 

 This evidence might be taken to suggest that poor nutrition depresses FSH 

 secretion. 



However, one thing that seems well established is that the ovulation rate 

 depends not only on the amount of hormone available for follicle growth 

 but also on the time available for its action. A change in ovulation rate is 

 not necessarily due to an altered quantity of secretion. 



There is a seasonal change in ovulation rate (1, 40, 47, 52) and this is not 

 of nutritional origin (59). The ovulation rate rises to a maximum at a time 

 when estrus is most intense and conception rate highest (1). The cycle length, 

 however, is not then at a minimum; on the contrary, there is a tendency for 

 the length to increase in the first part of the season (2, 40). 



Work at Cornell (45) shows the ovulatory release of hormone to be neuro- 

 genic and, in the cow, that it occurs after the start of heat. Either delay in 

 this release or advancement of the stimulus to follicle growth relative to 

 luteal regression might alter ovulation rate. 



There seems no reason to doubt that steroids act centrally in the induction 

 both of heat and of the ovulatory discharge from the pituitary. Quite apart 

 from the results of Clegg et al. (15) with hypothalamic lesions, the hormone 

 work on sheep would seem to indicate the points of action differ for the two 

 effects. Progesterone appears to antagonize estrogen at each, but possibly 

 the steroids interact differently at the two sites. 



The occurrence of silent heats after hormone treatment, or under poor 

 nutrition, might be due to factors of timing, or of level of estrogen secretion 

 under altered FSH : LH balance, or even of some adrenal corticoid antagon- 

 ism to heat but not to ovulation. 



Estrogen appears to provoke an explosive ovulatory discharge. The 

 discharge of hormone on progesterone withdrawal — which leads eventually 

 in some anestrous sheep to ovulation — initially must cause follicle growth 

 and is probably not similarly explosive. A sudden rise in hormone level seems 

 likely to impair the capacity of follicles to ovulate. If one considers how one 

 or two follicles gain an advantage over the rest, an initially slow, continuous 



