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Biology of Reproduction, Vol 24, 505-511, Copyright © 1981 by Society for the Study of Reproduction
1 Tulane University School of Medicine and the
Veterans Administration Medical Center,
New Orleans, Louisiana 70146 Immature female rats were treated with D-Trp6-LHRH to determine if the delay in vaginal
opening induced by the superactive agonist of LHRH could be correlated with changes in ACTH,
prolactin, or corticosterone levels. The rats were injected daily from Day 30 to Day 40 of age with
0.05 or 1 µg of D-Trp6-LHRH or with saline alone. Six animals per group were sacrificed on Days
31, 35, 38, or 42 and trunk blood collected. Pituitary and adrenal weights did not vary between
groups, but increased in all treatment regimens as the animals grew older. Prolactin and ACTH
levels increased on Days 35 and 38 in the control animals, but were significantly reduced in both
agonist-treated groups. Relative to controls, serum corticosterone was elevated (P<0.05) on Day 31
in 0.05 µg-treated animals and decreased on Day 38 in animals treated with 1 µg D-Trp6-LHRH.
The addition of corticosterone (160 µg/ml in 4% ethanol) to the drinking water reversed the
inhibitory effects of 1 µg of D-Trp6-LHRH on vaginal opening. In animals treated with saline or
0.05 µg D-Trp6-LHRH, corticosterone did not affect the normal vaginal opening. These results
demonstrate that it is possible that D-Trp6-LHRH delays vaginal opening through its effect on
corticosterone levels.
Accepted on November 20, 1980
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