Recent studies in male rats have shown that the number of pituitary gonadotropin-releasing hormone (GnRH) receptors is increased by castration and by injections of GnRH. This suggests that GnRH has a positive influence on the number of its own receptors, and that GnRH-binding capacity (GnRHBC) is related to the concentration of GnRH in portal blood. The present study was performed to determine if lesions of the medial basal hypothalamus would prevent the postcastration rise of pituitary GnRH receptors and whether exogenous GnRH administration to lesioned animals would maintain receptor numbers. In sham-lesioned castrate rats, the GnRH-BC increased progressively and was twice the basal level by 3 days after surgery. Large medial basal hypothalamic lesions completely eliminated this rise after castration but did not reduce GnRH-BC in intact (noncastrated) control animals. Serum LH levels were undetectable in lesioned rats, but serum PRL levels were elevated, indicating that the lesions had not damaged the pituitary. When native GnRH (6.6 μg, sc, every 8 h for 3 days) was administered to lesioned rats, the number of GnRH receptors increased in both intact and castrate animals to a similar value (360 ± 4 fmol/mg protein), but the receptor number was less than that in sham-lesioned castrates (550 ± 75 fmol/mg). The LH response to GnRH (last injection 1 h before decapitation) was greater in castrate than in intact lesioned rats despite similar concentrations of GnRH receptors. Since testosterone was elevated in the intact lesioned rats, this suggests that gonadal steroids can exert a negative feedback on pituitary LH secretion at a post-GnRH receptor locus. These results are consistent with the hypothesis that the rise in GnRH receptors after castration is a result of increased GnRH secretion, and suggest that the number of GnRH receptors reflect changes in GnRH secretion by the hypothalamus.
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Pieper et al. (1982) studied this question.