154 Richard M. Fraps 



thus intervenes, but since excitation hormone concentrations are assumed 

 to continue to increase during this period, the first excitation of the cycle. 

 El or El', takes place at relatively high threshold values. It is this circumstance 

 which, presumably, accounts for the relatively great extent of lag associated 

 with E2 and thus with lag in ovulation of the second follicle of the sequence 

 (Fig. 1). 



In this formulation of cyclic relationships, considerable emphasis has been 

 placed on the role of diurnal periodicity (or rhythmicity) in thresholds of 

 response in the neural component of the system (15-17). There can be little 

 doubt that some phase or phases of the prevailing photoperiod determine in 

 large measure the hours of the 24 within which nervous activation of the 

 pituitary for OIH release may normally occur. In this sense the meaning of 

 diurnal periodicity is reasonably clear. The supposition that, within this 

 period, thresholds of response vary with time of day introduces, however, 

 a notion of rhythmicity rather than of simple periodicity. The postulated 

 rhythmicity may be considered in part at least a characteristic of the "center" 

 exhibiting diurnal periodicity, or an expression mainly of ovarian (and 

 perhaps other) hormone actions on such a center. While in one form or 

 another it does seem necessary to postulate varying parameters of nervous 

 response to an excitation hormone, it is not supposed that the relationships 

 represented in Fig. 5 are the only ones possible. 



Estrogen 



Although the nature of the delaying action of exogenous estrogen on 

 ovulation of the C^ follicle contributed to formulation of the hypothesis 

 discussed above, it was not until the observation of a similar gonadotropin- 

 induced delay, presumably mediated through increased levels of endogenous 

 estrogen acting at a neural level, that the substance was seriously thought to 

 play a part in the appearance of lag (25). The normal OIH release represents 

 certainly an increase in circulating gonadotropin levels, whether of LH 

 alone or of the gonadotropic complex. We might reasonably expect such a 

 release to effect, as presumably did the injection of LH or of LH + FSH, an 

 increase in levels of circulating estrogen. There are also grounds, to be dis- 

 cussed later, for believing that the oviducal egg may stimulate estrogen pro- 

 duction during some 4 to 5 hr following its ovulation. However this may be, 

 estrogen levels in the regularly ovulating hen would appear to vary in a 

 pattern which is closely associated with the occurrence of OIH release. It 

 may be suggested then that relatively high estrogen levels so generated act 

 to suppress the appearance of low thresholds (or high sensitivity) in the neural 

 component of the OIH release mechanism. With subsequently decreasing 

 estrogen levels, at a time related to time of preceding OIH release (and possibly 

 the early oviducal egg), thresholds in the neural component would be expected 

 to fall and excitation to become possible. Each OIH release (and egg) except 



