158 Richard M. Fraps 



since the intervals between successive ovulations arc decreasing. In lengthy 

 sequences, recovery would proceed at the same, and at a relatively rapid rate, 

 not at onset of the sequence but during those phases in which lag approaches 

 or equals zero (Fig. 1). But supposing these and other aspects of recovery 

 within the sequence to be accounted for, there remains the formidable period 

 of lapse. We have seen earlier that through most or all of this period there 

 coexist an ovulable follicle and an apparently competent pituitary. If recovery 

 were indeed a decisive factor in pituitary function it would thus appear to 

 have been completed by about the same course as is assumed following 

 episodes of inhibition within the sequence. Yet the first ovulation of the 

 oncoming sequence occurs in association with the prevailing photoperiod, 

 many hours later than would be expected in terms of pituitary recovery. The 

 simple fact that ovulation of the Cj follicle does occur in close association 

 with some phase of photoperiod over a wide range of photoperiods (38) 

 would seem to cast doubt, apart from any other consideration, on the postu- 

 lated role of pituitary recovery during the period of lapse. 



One is certainly inclined to agree with Nalbandov that the oviducal egg 

 most probably does play a role in some aspect of the ovulation cycle. If the 

 hypotheses proposed by Nalbandov (42, 44) in this connection seem unsatis- 

 factory, we should perhaps inquire whether the experimental observations on 

 which these proposals are based have in fact been accounted for adequately, or 

 if not, whether more likely explanations can be suggested. 



The experimental oviducal irritant appears to maintain a gonadotropic 

 hormone balance similar in some important respects to that imposed by 

 the continuing administration of FSH or PMS (4). The daily injection of 

 such preparations in adequate quantities maintains follicular growth but 

 invariably interrupts ovulation after a day or two, thus resulting in a gradual 

 accumulation of ovulable follicles (28). Small follicles may also be caused to 

 grow more rapidly than usual, further increasing the mass of follicular tissue. 

 Under these conditions we should certainly expect higher than normal 

 estrogen levels, and it is not likely that these would show much diurnal 

 variation, certainly not under the pressure of daily PMS injections. On the 

 basis of evidence advanced earlier, the total suppression of 01 H release can 

 be attributed to these continuing high estrogen levels, and the site of estrogen 

 action would be in some neural component of the OIH release mechanism (25). 



In view of the fact that oviducal irritants and continuing gonadotropin 

 administration are similarly effective in suppressing OIH release, it may be 

 suggested that the oviducal irritant acts over neurogenic pathways to stimu- 

 late or to maintain those nervous activities, ordinarily periodic, which are 

 associated with the output of gonadotropins at a level favoring the secretion 

 of estrogen into the blood stream at concentrations capable of blocking 

 excitation for OIH release. In these terms, the oviducal irritant acts as a 

 stimulus at the neural level, and only secondarily in an inhibitory capacity. 



