Abstract

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-indueed PRL levels in the serum and PRL cOncentrations in the pituitary gland. Treatment with a moderate dose (1 pg/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�sg/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 11g/day) increased serum and pituitary PRL concentrations severalfold. However, neither testosterone nor EB treatment of orehideetomized 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 pg/day) decreased basal levels of GH in serum and prevented the usual posteastration 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.

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