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We recently found lumbosacral sympathetic ganglionic galanin neurons innervating the quail uterine oviduct. Galaninergic innervation of the uterine muscle may be essential for avian oviposition, as galanin evoked oviposition through a mechanism of induction of vigorous uterine contraction. The questions arising from these findings are: what changes occur in galanin expression in the sympathetic ganglionic galanin neuron during development, and what is the hormonal factor(s) that induces galanin expression in this neuron? Therefore, the present study examined the developmental changes in galanin of the quail sympathetic ganglionic neuron and uterus, and the effect of administration of ovarian sex steroids on galanin induction. Immature birds reared under long-day photoperiods from 4 weeks of age demonstrated progressive increases in galanin levels both per unit ganglionic protein (concentration) and per ganglia (content) concurrent with ganglionic development during weeks 4--13. The uterine galanin content and uterine weight also increased progressively during the same period, but the galanin concentration in the uterus at 4 weeks was high due to the much smaller tissue mass. Immunocytochemical analysis with anti-galanin serum showed that immunoreactive ganglionic cells were few and small at 4 weeks and increased progressively thereafter. Administration of oestradiol-17 beta to immature birds at 3 weeks of age for 1 week increased both the galanin concentration and content in the ganglia without ganglionic growth. A marked increase in galanin-immunoreactive ganglionic cells was detected following oestradiol treatment. In contrast, progesterone increased ganglionic galanin levels, but the effects were low. Expression of the mRNAs encoding oestrogen receptor-alpha and -beta (ER alpha and ER beta) in the ganglionic tissue was verified by RT-PCR/Southern blot analysis. Immunocytochemical staining with anti-ER serum further revealed an intense immunoreaction restricted to the nucleus of ganglionic neurons. These results suggest that ovarian sex steroids, in particular oestradiol-17 beta, contribute as hormonal factors to galanin induction, which takes place in the lumbosacral sympathetic ganglionic neurons innervating avian uterine oviduct during development. Oestradiol may act directly on this ganglionic neuron through intra-nuclear receptor-mediated mechanisms to induce galanin.
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In this work we determined progesterone receptor (PR) mRNA content in female rabbit lung during the first 5 days of pregnancy and in ovariectomized animals after subcutaneous injection of oestradiol benzoate (25 micrograms/kg) for 2 days or oestradiol benzoate (25 micrograms/kg) for 2 days plus a single dose of progesterone (5 mg/kg) on day three. On each day (0-5) of pregnancy and 24 h after the last dose in the case of the treated animals, animals were killed and lung was excised; total RNA was extracted and processed for Northern blot analysis. The results showed three main PR mRNA transcripts (6.1, 4.4 and 1.8 kb) in rabbit lung. The 4.4 kb species was the most abundant. PR mRNA content was markedly increased by oestradiol benzoate and downregulated by progesterone. It significantly increased on the first day of pregnancy and then diminished progressively, reaching its lowest value on day 5. These findings suggest that PR mRNA content in the rabbit lung is regulated by sex steroid hormones and changes according to the physiological concentrations of oestradiol and progesterone.
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. doi:10.1016/0002-9149(92)91300-S . Iverius PH Brunzell JD 1988 Relationship between lipoprotein lipase activity and plasma sex steroid level in obese women . Journal of Clinical Investigation 82 1106 – 1112 . doi:10.1172/JCI113667 . Jones
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sexually experienced copulating males, currently no data are available on the hormonal signals triggering this phosphorylation and its functional relevance. We first focused on the role of sex steroid hormones as the mPOA highly expresses AR ( Raskin et
Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA
The Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA
Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, Pennsylvania 19111, USA
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Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA
The Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA
Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, Pennsylvania 19111, USA
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Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA
The Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA
Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, Pennsylvania 19111, USA
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Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA
The Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA
Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, Pennsylvania 19111, USA
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Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA
The Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA
Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, Pennsylvania 19111, USA
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the concentration that enters the salivary gland but also that available to other tissues. In contrast, the major fraction of plasma sex steroids are strongly bound to their respective binding globulins and concentrations are normally reported as the
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ABSTRACT
The role of sex steroids in the programming of the level of serum corticosteroid-binding globulin (CBG) in the rat has been studied at different stages of ontogenesis.
The CBG content in the serum of mature female rats was 2·5 times higher than that in male rats. Sexual dimorphism of CBG content was absent in immature animals of 3–4 weeks of age. Castration of mature rats led to a 40–50% increase in CBG content. The CBG concentration in mature females or castrated adult males treated with testosterone propionate (TP; 3 mg/day for 4 days) was decreased by 40–50% compared with vehicle-treated rats. Oestradiol injection (1 μg/day for 4 days) had no influence on CBG levels in mature male and ovariectomized adult female rats.
Immature rats were castrated on days 1, 7, 14, 21, 28 or 35 of age and the CBG level was determined at 10–12 weeks of age. The CBG content of rats castrated up to day 28 of age was 2·5 times higher than that in mature males and did not differ from that in mature females. The CBG content of male rats castrated on day 35 of age was the same as that of adult castrated males. The CBG level in castrated rats treated with TP (1·25 mg for days 1–3 or 300 μg/day for 5 days after castration at day 7 up to day 26) did not differ from that in controls (i.e. vehicle-treated rats). TP injection into castrated rats on days 29–33 of age (300 μg/day) led to a 40–50% decrease in CBG level when compared with controls.
Ovariectomy of rats at different ages (on days 1 or 28 or 3 months) did not affect CBG concentration. TP injection (300 μg/day) into ovariectomized rats on days 29–33 had the same effect on CBG concentration as in males.
Gonadectomized rats treated with diethylstilboestrol on days 29–33 (100 μg/day) had the same CBG concentrations as TP-treated rats.
It was concluded that there is a short period during ontogenesis, from days 29 to 35 of age, which is critical for irreversible masculinization of the CBG concentration in male rats.
Journal of Endocrinology (1992) 132, 235–240
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Concentrations of sex steroid-binding protein (SBP) in plasma of immature male little brown bats (Myotis lucifugus lucifugus) were found to be low (15 ± 2·8 (s.e.m.) nmol/l) and stable throughout the period of hibernation which immediately precedes the onset of the first spermatogenic cycle (sexual maturity). In contrast, plasma SBP titres in spermatogenically active adults (summer) were markedly raised (238 ± 26 nmol/l). When immature males were removed from hibernation and maintained on a long photoperiod of 16 h light: 8 h darkness at a constant temperature of 25 °C to accelerate the onset of sexual maturity, these animals exhibited a rapid rise in circulating SBP. Plasma levels of SBP in immature males maintained on a long photoperiod increased significantly after 2 weeks, and by 3 weeks reached values (234± 20 nmol/l) that were indistinguishable from those seen in spermatogenically active adults. These high plasma SBP titres at 3 weeks were accompanied by increases in testicular and epididymal weights and the onset of spermatogenesis. However, no stimulation of the sex accessory glands was observed, possibly reflecting the effects of increased plasma SBP on the biological activity of circulating androgens. The ability of immature male Myotis to exhibit a pubertal increase in plasma SBP following simple environmental manipulation should provide a valuable model for the study of the control and action of sex steroid-binding protein.
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In this study we used an isolation/restraint stress to test the hypothesis that stress will affect the secretion of LH differently in gonadectomised rams and ewes treated with different combinations of sex steroids. Romney Marsh sheep were gonadectomised two weeks prior to these experiments. In the first experiment male and female sheep were treated with vehicle or different sex steroids for 7 days prior to the application of the isolation/restraint stress. Male sheep received either i.m. oil (control rams) or 6 mg testosterone propionate injections every 12 h. Female sheep were given empty s.c. implants (control ewes), or 2x1 cm s.c. implants containing oestradiol, or an intravaginal controlled internal drug release device containing 0.3 g progesterone, or the combination of oestradiol and progesterone. There were four animals in each group. On the day of application of the isolation/restraint stress, blood samples were collected every 10 min for 16 h for the subsequent measurement of plasma LH and cortisol concentrations. After 8 h the stress was applied for 4 h. Two weeks later, blood samples were collected for a further 16 h from the control rams and ewes, but on this day no stress was imposed. In the second experiment, separate control gonadectomised rams and ewes (n=4/group) were studied for 7 h on 3 consecutive days, when separate treatments were applied. On day 1, the animals received no treatment; on day 2, isolation/restraint stress was applied after 3 h; and on day 3, an i. v. injection of 2 microg/kg ACTH1-24 was given after 3 h. On each day, blood samples were collected every 10 min and the LH response to the i.v. injection of 500 ng GnRH administered after 5 h of sampling was measured. In Experiment 1, the secretion of LH was suppressed during isolation/restraint in all groups but the parameters of LH secretion (LH pulse frequency and amplitude) that were affected varied between groups. In control rams, LH pulse amplitude, and not frequency, was decreased during isolation/restraint whereas in rams treated with testosterone propionate the stressor reduced pulse frequency and not amplitude. In control ewes, isolation/restraint decreased LH pulse frequency but not amplitude. Isolation/restraint reduced both LH pulse frequency and amplitude in ewes treated with oestradiol, LH pulse frequency in ewes treated with progesterone and only LH pulse amplitude in ewes treated with both oestradiol and progesterone. There was no change in LH secretion during the day of no stress. Plasma concentrations of cortisol were higher during isolation/restraint than on the day of no stress. On the day of isolation/restraint maximal concentrations of cortisol were observed during the application of the stressor but there were no differences between groups in the magnitude of this response. In Experiment 2, isolation/restraint reduced the LH response to GnRH in rams but not ewes and ACTH reduced the LH response to GnRH both in rams and ewes. Our results show that the mechanism(s) by which isolation/restraint stress suppresses LH secretion in sheep is influenced by sex steroids. The predominance of particular sex steroids in the circulation may affect the extent to which stress inhibits the secretion of GnRH from the hypothalamus and/or the responsiveness of the pituitary gland to the actions of GnRH. There are also differences between the sexes in the effects of stress on LH secretion that are independent of the sex steroids.
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ABSTRACT
The incubation of female rat adenohypophysial cells in primary culture with porcine granulosa cell culture medium (GCM) led to the complete inhibition of responses of LH and FSH to LH releasing hormone (LHRH) as well as to the inhibition of spontaneous release of FSH. These effects of GCM suggest the specificity of the 'inhibin'-like activity of this material. Granulosa cell culture medium completely reversed the stimulatory effect of oestradiol-17β on the responses of LH and FSH to LHRH, as well as reversing the stimulatory effect of progesterone, oestradiol or a combination of both steroids on the spontaneous release of FSH, while not affecting the spontaneous release of LH. The antioestrogenic effects of progesterone observed on the response of LH to 0·3 nm-LHRH were amplified in the presence of GCM while the stimulatory effects of progesterone, oestradiol or both on the response of FSH to 0·3 nm-LHRH were completely reversed by the medium. Moreover, the presence of GCM led to an additive inhibitory effect with dihydrotestosterone on the response of LH to LHRH while it completely reversed the stimulatory effect of the androgen on spontaneous and LHRH-induced FSH release. The present data show that the presence of porcine granulosa cell 'inhibin' activity can exert marked interactions with sex steroids in the control of gonadotrophin secretion. This 'inhibin' activity reversed all the stimulatory effects and potentiated all the inhibitory effects of sex steroids on gonadotrophin secretion. Although the physiological role of 'inhibin' remains to be defined well, the importance of this activity is clearly demonstrated in anterior pituitary cells in culture.
J. Endocr. (1984) 100, 133–140
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ABSTRACT
11β-Hydroxysteroid dehydrogenase (11β-OHSD) catalyses the reversible conversion of corticosterone to inactive 11-dehydrocorticosterone, thus regulating glucocorticoid access to mineralocorticoid and perhaps glucocorticoid receptors in vivo. 11β-OHSD has been purified from rat liver and an encoding cDNA isolated from a liver library. However, several lines of indirect evidence suggest the existence of at least two isoforms of 11β-OHSD, one found predominantly in glucocorticoid receptor-rich tissues and the other restricted to aldosterone-selective mineralocorticoid target tissues and placenta. Here we have examined the effects of chronic (10 day) manipulations of sex-steroid levels on 11β-OHSD enzyme activity and mRNA expression in liver, kidney and hippocampus and present further evidence for the existence of a second 11β-OHSD isoform in kidney.
Gonadectomized male and female rats were given testosterone, oestradiol or blank silicone elastomer capsules, controls were sham-operated. In male liver, gonadectomy+ oestradiol treatment led to a dramatic decrease in both 11β-OHSD activity (69 ± 8% decrease) and mRNA expression (97 ± 1% decrease). Gonadectomy and testosterone replacement had no effect on male liver 11β-OHSD. However, in female liver, where 11β-OHSD activity is approximately 50% of that in male liver, gonadectomy resulted in a marked increase in 11β-OHSD activity (120 ± 37% rise), which was reversed by oestradiol replacement but not testosterone treatment.
In male kidney, gonadectomy+oestradiol treatment resulted in a marked increase in 11β-OHSD activity (103 ± 4% rise). By contrast, 11β-OHSD mRNA expression was almost completely repressed (99 ± 0·1% decrease) by oestradiol treatment. This effect of oestradiol was reflected in a loss of 11β-OHSD mRNA in all regions of the kidney showing high expression by in-situ hybridization. In female kidney, oestradiol replacement also led to an increase in 11β-OHSD activity (70 ± 15% rise) while mRNA expression fell by 95 ± 3%. None of the treatments had any effect on enzyme activity or mRNA expression in the hippocampus, although transcription starts from the same promoter as liver.
We conclude that (i) sex steroids regulate 11β-OHSD enzyme activity and mRNA expression in a tissue-specific manner and (ii) the concurrence of increased enzyme activity with near absent 11β-OHSD mRNA expression in the kidney following oestradiol treatment suggests that an additional gene product is responsible, at least in part, for the high renal activity observed.
Journal of Endocrinology (1993) 139, 27–35
