Stress and its adrenal involvement has been suggested 
of accounting for the lowered reproduction rates observed in 
animal populations living under crowded stressed conditions. 
The pituitary increases its output of A.C.T.H. and stimulates 
the adrenal to increasing production of glucocorticoids. Due 
to the increased A.C.T.H. output, the pituitary shifts and ree 
duces its output of other hormones such as the gonadotropins. 
Seigel (1959) tried to test this theory with White Leghorn 
pullets. He found over a 196-day period significantly lower: 
egg production from the group confined to 1.353 sqe ft. per bird 
as compared to those with 4.00 sq. ft. per bird. The number of 
birds per group laying was not reduced, but the number of eggs 
per bird and the mean cycle length were significantly reduced. 
Berry and Payne in 1961 showed a pineal body and 
thymus gland effect on egg production. They removed at four days 
of age wither the pineal body, thymus gland or both. Péneal- 
ectomized birds laid significantly fewer eggs than either other 
group. Thymectomized birds laid at the highest rate, whereas 
removal of both glands resulted in production almost equal to 
simple thymus removal. No suggestive reasons were given. | 
Huston and Nalbandov (1950) showed that suspending 
coarse surgical thread, glass beads, paraffin balls, or pieces 
of cork in the lumen of the oviduct resulted in the bird ceasing 
to lay while, however, the follicular growth continued in the 
ovaries. The same operation on immature females delayed or pre- 
vented thelr sexual maturity. While objects were in the oviduct, 
injections of progesterone or L.H. caused ovulation as long as 
the injections continued (Huston and Nalbandov, 1953). ‘The 
irritant seemed to prevent the secretion of L.H. sufficiently 
to cause ovulation. This would suggest the existence of a 
neurogenic control system between the oviduct and pituitary. 
Ralph and Fraps (1960) induced premature ovulation in 
hens by injecting progesterone into certain regions of either 
the hypothalamus or the caudal neostriatum, but not by a 
in other parte of the forebrain or pituitary. They (1959 
placed electrolytic lesions at various sites within the hypo- 
thalamus of birds previously injected with progesterone and 
found that only those lesions within a ventro-median portion of 
the. preoptic hypothalamus, or along fiber tracts passing caudal 
from this region regularly prevented ovulation that ordinarily 
would have been induced. If lesions were placed within two hours 
after injection, ovulation was prevented; after this time, it 
only prevented or delayed subsequent ovulation. van Tienhoven, 
Nalbandov and Norton (1954) showed that dibenamine was capable 
of blocking spontaneous as well as progesterone induced ovulation. 
It blocked mest effectively 14 hours before ovulation, suggest- 
ing that the hen's L.H. is released 8 to 14 hours before ovula- 
tion. Conner and Fraps (1955) showed that phenobarbital sodium 
injected 22=43 hours before initial ovulation and 17-23 hours 
before second ovulation caused a high proportion of suppressed 
ovulations. In nearly every case of suppressed ovulation, 
58 
