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Gonadotropin-Releasing Hormone Messenger Ribonucleic Acid Levels Are Unaltered with Changes in the Gonadal Hormone Milieu of the Adult Male Rat^*

Departments of Obstetrics and Gynecology (D.K.C, R.A.S.), Physiology and Biophysics (J.N. W., R.A.S.), Zoology (R.A.S.), and the Population Center for the Study of Reproduction (D.K.C, R.A.S.), University of Washington Seattle, Washington 98195

Address correspondence and requests for reprints to: Robert A. Steiner, Department of Obstetrics and Gynecology RH-20, University of Washingotn, Seattle, Washington 98195.

Abstract

Testicular function is regulated by the negative feedback effect of sex hormones acting at the brain and pituitary to inhibit the secretion of LH and FSH. An important component of this feedback axis is presumed to involve regulation of secretion and possibly synthesis of GnRH by the brain. We tested the hypothesis that the castration-induced increase in gonadotropin secretion is subserved, at least in part, by increased synthesis of GnRH. Using in situ hybridization and an oligonucleotide probe to pro-GnRH messenger RNA (GnRH mRNA), we compared the level of cellular GnRH mRNA and the relative number of GnRH mRNA-containing neurons between intact and 21-day castrate adult male rats. To derive estimates of the number of GnRH cells and the cellular GnRH mRNA content, coronal sections from each animal were anatomically matched between intact and castrate groups. All identifiable cells within these sections were counted and analyzed with the aid of a computerized image analysis system, by an observer unaware of the animal's experimental group and were assigned an anatomical location for reference.

In an initial experiment, we observed no difference in cellular GnRH mRNA signal level between intact (n = 4) and castrate (n = 5) animals (129 ± 8 vs. 139 ± 5 grains per cell); however, we did find a statistical difference between the intact and castrated groups in the relative number of GnRH mRNA-containing cells (intact: 212 ± 15 vs. castrate: 320 ± 18). To confirm this observation, we repeated the experiment by again comparing the number of GnRH mRNA-positive cells between intact (n = 4) and castrate (n = 4) rats. In this second experiment, we found no difference in the number of identifiable GnRH mRNAcontaining cells between intact and castrate animals (272 ± 14 vs. 274 ± 36, respectively); this was the case for the total cell count as well as when the data were analyzed by anatomical region. To clarify the conflicting results on cell counts of Exps 1 and 2, we repeated the experiment a third time, again comparing both the number of GnRH mRNA-containing cells and the cellular content of GnRH mRNA. In this experiment, we observed that neither cell number nor content of GnRH mRNA differed between the intact and castrate groups. Again, this was the case for total cell count, as well as when the data were analyzed by anatomical region. In a fourth experiment, instead of the oligonucleotide probe we had used in the previous 3 experiments, we developed a cloned complementary RNA probe to the prepro-GnRH message and applied this with in situ hybridization to address the same question. In this experiment, as in 2 of the previous experiments, we observed no difference in either GnRH mRNA-positive cell number (intact: 136 ± 6 us. castrate: 126 ± 6) or cellular GnRH mRNA signal level (intact: 169 ± 7 vs. castrate: 158 ± 7 grains per cell) between the intact and castrate groups. Moreover, in this, as in the previous 2 experiments when the data were analyzed by anatomical region, no difference in either cell number or message content was detected between groups. These results confirmed the findings of Exps 1 and 3 with respect to cellular GnRH mRNA content and corroborate the findings of Exps 2 and 3 for cell count. We conclude that neither the number of GnRH mRNA-positive cells nor the cellular GnRH mRNA content is altered after long term castration in the adult male rat, suggesting that feedback control of gonadotropin secretion does not depend upon compensatory changes in GnRH biosynthesis. (Endocrinology 127: 523–532, 1990)

Footnotes

^* This research has been supported by NIH Grants HD-12629 and HD-12625.

Received March 22, 1990.

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