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Biology of Reproduction, Vol 21, 473-481, Copyright © 1979 by Society for the Study of Reproduction
1 Lutcher Brown Center for Diabetes and Endocrinology,
Scripps Clinic and Research Foundation,
La Jolla, California 92037 The influences of castration and of subsequent replacement therapy with gonadal hormones on
the secretion of prolactin (PRL) and growth hormone (GH) in male and female mice were investigated. Long term castration in female mice significantly reduced basal and perphenazine-induced
PRL levels in the serum and PRL concentrations in the pituitary gland. Treatment with a moderate
dose (1 µg/day) of estradiol benzoate (EB) for several weeks increased PRL levels in the pituitary
gland and serum, but the release of PRL in response to perphenazine was not augmented. A large
dose of EB(20 µg/day), on the other hand, resulted in a smaller increase in pituitary concentrations,
little or no increase in basal serum levels and complete abolition of perphenazine-induced PRL
release, suggesting that high doses of EB are detrimental to the release of PRL. In male mice, castration had little or no effect on PRL levels in the pituitary gland or on basal
concentrations in serum, but it significantly reduced perphenazine-induced release of PRL. Administration of testosterone (0.5 mg/day) only marginally enhanced pituitary and serum concentrations
of PRL, whereas EB injection (1 µg/day) increased serum and pituitary PRL concentrations severalfold. However, neither testosterone nor EB treatment of orchidectomized males could cause serum
PRL concentrations to rise after injection of perphenazine to levels equivalent to those in intact
females. This suggests that the sex difference in the control of PRL secretion in adult mice involves
the pituitary-hypothalamic system rather than the gonad. Concentrations of GH in the pituitary glands and sera of female mice increased following castration, whereas administration of EB (1 µg/day) decreased basal levels of GH in serum and prevented
the usual postcastration rise in serum and pituitary GH. In male mice, in contrast, castration
reduced pituitary GH concentrations but had no marked influence on serum GH. Administration
of testosterone (0.5 mg/day), in turn, increased pituitary GH concentrations, with no appreciable
influence on serum GH. These results indicate that the female gonad exerts a net inhibitory influence on GH secretion in female mice, whereas, although essential for maintaining normal levels in
the pituitary gland, the male gonad has little influence on the circulating levels of GH in male mice.
Note:
ACKNOWLEDGMENTS
Supported by grants CA-14025 and CA-18664,
awarded by the National Cancer Institute, DHEW.
This is Publication No. 7 from the Lutcher Brown
Center for Diabetes and Endocrinology. A preliminary
report of part of this work has appeared in abstract
form (Program 59th Meeting, Endocrine Society,
1977, p. 224).
This article has been cited by other articles:
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  J. F. Couse, M. M. Yates, V. R. Walker, and K. S. Korach Characterization of the Hypothalamic-Pituitary-Gonadal Axis in Estrogen Receptor (ER) Null Mice Reveals Hypergonadism and Endocrine Sex Reversal in Females Lacking ER{alpha} But Not ER{beta} Mol. Endocrinol., June 1, 2003; 17(6): 1039 - 1053. [Abstract] [Full Text] [PDF]
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