Testosterone regulates the secretion of thyrotrophin-releasing hormone (TRH) and TRH precursor in the rat hypothalamic-pituitary axis

1990 ◽  
Vol 125 (2) ◽  
pp. 263-270 ◽  
Author(s):  
A. E. Pekary ◽  
M. Knoble ◽  
N. H. Garcia ◽  
S. Bhasin ◽  
J. M. Hershman
Keyword(s):  
In Vitro Release ◽  
Serum Levels ◽  
Male Rats ◽  
Testosterone Replacement ◽  
Male Rat ◽  
Posterior Pituitary ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Vitro Release

ABSTRACT Orchidectomy has been reported to decrease concentrations of thyrotrophin (TSH) in the circulation of male rats without affecting serum levels of thyroid hormones. To understand the mechanism underlying this observation, we have measured the effect of gonadal status on the in-vitro release of TSH-releasing hormone (TRH) by male rat hypothalamic fragments. Because hormone release rates can be affected by changes in the post-translational processing of the hormonal precursors, we have also studied the corresponding changes in the concentrations of TRH and TRH-Gly, a TRH precursor peptide in hypothalamus and pituitary, by radioimmunoassay. We observed a significant decline in the in-vitro release of TRH from incubated hypothalami 1 week after castration, which was quantitatively reversed by testosterone replacement. Concentrations of TRH and TRH-Gly in the posterior pituitary, on the other hand, which derive from neurones of hypothalamic origin, increased significantly with castration and were returned to the normal range by testosterone replacement. We conclude that the primary effect of testosterone is the stimulation of hypothalamic TRH release, resulting in the depletion of TRH and TRH precursors from TRH-containing neurones which project into the median eminence and posterior pituitary. Journal of Endocrinology (1990) 125, 263–270

Effect of starvation on gonadotrophin secretion and on in vitro release of LRH from the isolated median eminence of the male rat

1983 ◽  
Vol 103 (3) ◽  
pp. 293-301 ◽  
Author(s):  
Michael Warnhoff ◽  
Gunter Dorsch ◽  
Karl M. Pirke
Keyword(s):  
In Vitro Release ◽  
Basic Mechanism ◽  
Male Rat ◽  
Gonadotrophin Secretion ◽  
Significant Difference ◽  
Lh Release ◽  
And Control ◽  
Vitro Release

Abstract. A perfusion system was developed in which isolated median eminences (ME) were stimulated in vitro by depolarizing agents such as potassium and veratridine. Potassium concentrations between 30 and 80 mm released increasing amounts of luteinizing hormone-releasing hormone (LRH) from the MEs of starved and control rats. Veratridine at a concentration of 50 μm caused a more prolonged LRH release in both starved and control animals. LRH secretion in vitro was slightly, though not under all conditions, significantly greater in rats starved for 5 days. The testosterone (T)-LH feedback was studied by castrating the animals and substituting various doses of T through implantation of T-releasing capsules of different sizes. The concentration in plasma, which can prevent the castration-induced much smaller in starved than in control rats. The in vitro release of LRH evoked by 80 mm potassium was not different for starved and fed rats under various feedback conditions. Both groups revealed decreased in vitro release of LRH when castrated animals were not substituted with T. The effect of castration was studied from 1 to 28 days. The plasma LH values rapidly increased in starved and control animals, indicating that the hypothalamic responsestration is not delayed by starvation. The release in vitro of LRH decreased from the first to the fifth day and remained constant thereafter. No significant difference between starved and fed rats was observed. The experiments indicate that the 'releasable pool' of LRH in vitro is greater under conditions of reduced LH release in vivo. The basic mechanism of depolarization-induced exocytosis of LRH from the ME is intact in starved animals.

scholarly journals Testosterone-dependent variations in plasma and intrapituitary corticosteroid binding globulin and stress hypothalamic-pituitary-adrenal activity in the male rat

2004 ◽  
Vol 181 (2) ◽  
pp. 223-231 ◽  
Author(s):  
V Viau ◽  
MJ Meaney
Keyword(s):  
Feedback Regulation ◽  
High Plasma ◽  
Male Rats ◽  
Testosterone Replacement ◽  
Male Rat ◽  
Plasma Testosterone ◽  
Hypothalamic Pituitary Adrenal ◽  
Corticosteroid Binding Globulin ◽  
Low Testosterone

Hypothalamic-pituitary-adrenal (HPA) activity is governed by glucocorticoid negative feedback and the magnitude of this signal is determined, in part, by variations in plasma corticosteroid-binding globulin (CBG) capacity. Here, in gonadectomized male rats we examine the extent to which different testosterone replacement levels impact on CBG and HPA function. Compared with gonadectomized rats with low testosterone replacement ( approximately 2 ng/ml), plasma adrenocorticotropin and beta-endorphin/beta-lipotropin responses to restraint stress were reduced in gonadectomized rats with high testosterone replacement ( approximately 5 ng/ml). Plasma CBG levels also varied negatively as a function of testosterone concentration. Moreover, glucocorticoid receptor binding in the liver was elevated by higher testosterone replacement, suggesting that testosterone acts to enhance glucocorticoid suppression of CBG synthesis. Since pituitary intracellular CBG (or transcortin) is derived from plasma, this prompted us to examine whether transcortin binding was similarly responsive to different testosterone replacement levels. Transcortin binding was lower in gonadectomized rats with high plasma testosterone replacement ( approximately 7 ng/ml) than in gonadectomized rats with low testosterone replacement ( approximately 2 ng/ml). This testosterone-dependent decrease in pituitary transcortin was associated, in vitro, with an enhanced nuclear uptake of corticosterone. These findings indicate that the inhibitory effects of testosterone on corticotrope responses to stress may be linked to decrements in plasma and intrapituitary CBG. This could permit greater access of corticosterone to its receptors and enhance glucocorticoid feedback regulation of ACTH release and/or proopiomelanocortin processing.

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