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Department of Cell Biology, Baylor College of Medicine Houston, Texas 77030;
Peptide Biology Laboratory, Salk Institutes San Diego, California 92138
Address requests for reprints to: Dr. Lutz Birnbaumer, Department of Cell Biology, Baylor College of Medicine, Texas Medical Center, Houston, Texas 77030.
Abstract
The possibility that GnRH or a GnRH-like material of ovarian origin may play a physiological role in follicular development was explored in immature hypophysectomized rats by testing whether a potent synthetic antagonist of GnRH action ([iV-acetyl-dehydro-Pro1,D-p-chloro-Phe2,D-Trp3-6]GnRH), would potentiate FSH-induced maturation of ovarian follicles to an ovulable stage. Rats were hypophysectomized on day 25 of their life and implanted with a Silastic capsule containing diethylstilbestrol. On day 30, they were started on injections of 10 ng NIH FSH-S12 twice daily alone (control) or in combination with 10 ng of either native GnRH or GnRH antagonist. On day 35, all rats received 30IU hCG to trigger ovulation and luteinization of mature follicles. Rats were killed 25.5-28 h later and inspected for number of ova in Fallopian tubes, ovarian weight, number of corpora lutea (CL) on ovarian surface, and appearance of hematoxylin- eosin-stained ovarian slices. In control animals (n = 6), we found some ovulations (mean ± SEM, 3.2 ± 1.1/rat), many more CL (16.5 ± 4.5/rat), and ovarian weights of 37.7 ± 1.1 mg/ rat. In GnRH-treated rats (n = 5), there were no CL formed, no ova were found, and ovarian weights were 16.0 ±1.5 mg/rat. In contrast, in GnRH antagonist-treated rats (n = 5), 16.4 ± 1.6 ova/rat were recovered from the Fallopian tubes, and ovaries contained 20.8 ± 2.5 CL/rat and weighed 52.7 ± 3.2 mg/rat. All changes were statistically significant. We conclude that an antagonist of GnRH action is able to potentiate the action of FSH on ovarian follicle development and suggest that it does so by inhibiting the action of an endogenous GnRH or GnRH-like substance that may play a role as a physiological atretic signal. (Endocrinology 116: 1367-1370,1985)
Footnotes
* This work was supported in part by NIH Grant HD-09581.
Received September 11, 1984.
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