Ovulation in the Domestic Fowl 157 



likewise suppress the periodic LH release required for ovulation. On this view, 

 neurogenic inhibition of the ovulatory LH release mechanism ceases when the 

 egg clears the magnum (or isthmus) and "LH is secreted in sufficient quantities 

 to cause the next ovulation" (42). 



In a recent reconsideration of the problem, Nalbandov (44) points out 

 that the period during which the neurogenic stimulus may act is no more 

 than about 5 hr following ovulation. In the two-member sequence, the 5-hr 

 period following ovulation of the C^ follicle would thus end 15-16 hr before 

 OIH release for ovulation of the second follicle, assuming 8 hr to elapse 

 between OIH release and ovulation. Even supposing an improbable 14-hr 

 interval between OIH release and ovulation, the neurogenic stimulus would 

 cease 9-10 hr before the second release of OIH in the 2-member sequence. 

 In the light of such considerations and, in addition, the failure of the earlier 

 hypothesis to account for the period of lapse, Nalbandov (44) recently pro- 

 posed a different interpretation of effects of the neurogenic stimulus (or 

 inhibition) from the oviduct. 



The hypothesis now proposed rests on several related propositions. Light 

 is believed not to regulate "rhythmicity of the laying cycle of birds", although 

 it does determine rate of pituitary function and thus has a "permissive 

 effect" on reproductive performance. The bird's pituitary is assumed to 

 secrete a single gonadotropic complex with FSH- and LH-like properties 

 rather than the two separate entities usually assumed. Secretion of this com- 

 plex is suppressed during passage of the egg through the magnum and 

 isthmus of the oviduct, a period of some 4-5 hr. Secretion of the gonadotropic 

 complex is resumed when the egg clears the isthmus and circulating gonado- 

 tropin slowly returns to pre-inhibition levels; with attainment of these levels, 

 ovulation is induced. 



Of these several assumptions, the crucial one with respect to the timing of 

 ovulation is clearly that of pituitary recovery following the 5-hr period of 

 inhibition. As stated by Nalbandov, sequence length "would be determined 

 by the rate at which the pituitary gland could recover from each episode of 

 neural inhibition. Thus, rapid recovery would permit long clutches, while 

 slow recovery would result in short clutches." The period of lapse is accounted 

 for similarly: "With each succeeding cycle of inhibition and release hypo- 

 physial recovery rate becomes slower until at the end of the clutch the 

 pituitary gland does not recover in time to cause the ovulation of the next egg, 

 and the clutch is interrupted." 



Several implications of the concept of pituitary recovery following episodes 

 of inhibition may be noted. Rate of recovery would plainly have to be very 

 finely adjusted to account for lag relationships seen in the ordinary ovulation 

 sequence, an improbable demand upon "recovery" in any guise. In sequences 

 of three or more members, rate of recovery would actually increase, not 

 decrease, with the several successive episodes of inhibition following the first, 



