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P. MacKinnon
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C. Clark
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E. M. Clement
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R. Sheaves
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ABSTRACT

The presence of adrenaline within the central nervous system appears to be essential for the occurrence of an oestrogen-stimulated surge of LH in both pro-oestrous and ovariectomized rats. Previous measurements of adrenergic activity based on the rate of decline of adrenaline (RDA) 2 h after injection of a synthesis inhibitor (SKF 64139) suggested that adrenergic activity increases in both the medial preoptic area (MPOA) and the mediobasal hypothalamus (MBH) at the start of the LH surge (15.00–17.00 h). The purpose of the present studies was to see whether oestrogen and progesterone affected this increase in adrenergic activity at the sites of the cell bodies (MPOA) and axon terminals (MBH) of the gonadotrophin-releasing hormone-synthesizing neurone. Rats ovariectomized at dioestrus showed a reduction in both plasma LH concentrations and RDA (P < 0·01) in the MBH between 15.00 and 17.00 h on the day of expected pro-oestrus. Oestrogen replacement at operation restored LH levels and the RDA to values found in intact rats. Injection of an antioestrogen (Cl-628), with or without oestrogen, also reduced plasma LH levels and the RDA (P < 0·01) in the MBH. Removal or replacement of oestrogen apparently had little effect on the RDA in the MPOA. In ovariectomized oestrogen-primed rats an injection of progesterone on the morning of expected pro-oestrus advanced and enhanced not only the LH surge but also the RDA in the MBH (P< 0·001). Moreover, concentrations of adrenaline in the MBH (but not the MPOA) decreased (P < 0·001) consistently over a 2-h period following injection of progesterone. These results support the suggestion that steroid-stimulated adrenergic activity in the MBH may be concerned with the preovulatory release of gonadotrophins.

J. Endocr. (1985) 104, 129–135

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E. M. Clement
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P. C. B. MacKinnon
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R. Sheaves
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ABSTRACT

In the mediobasal hypothalamus (MBH) of prooestrous rats or acutely ovariectomized oestrogentreated adults a marked but short-lived increase in adrenergic activity occurs at 16.00 h, 2 h before the oestrogen-dependent surge of gonadotrophins at 18.00 h. In this study oestrogen-stimulated (noon on day 1) 22-day-old female rats were used which are known to produce surge levels of prolactin at 18.00 h on day 2 and surges of both prolactin and LH at 18.00 h on day 3; although similar treatment of 18-day-old animals or oil-treated 22-day-old rats failed to produce these effects. Radioenzymatic assays of adrenaline concentrations and of the activity of its synthesizing enzyme (phenylethanolamine-N-methyl transferase; PNMT, EC 2.1.1.28) in the MBH of oestrogen-treated 22-day-old rats showed significant (P< 0·05–0·01) increases in both parameters at 16.00 h (i.e. 2 h before surge levels of gonadotrophins) on days 2 and 3 when compared with other times of day. Such effects were not seen in oil-treated 22-day-old animals or in oestrogen-treated 16-day-old rats. Noradrenaline and dopamine concentrations in the MBH of oestrogen-treated 22-day-old rats remained at baseline levels on days 2 and 3 with the exception of noradrenaline at 17.00 h on day 3 when levels appeared higher (P<0·05) than at either 15.00 or 16.00 h. Subsequent measurements of PNMT activity in oestrogen-treated 22-day-old rats at 4-hourly intervals throughout days 2 and 3 showed the presence of a clear circadian rhythm with peak levels occurring at 16.00 h. In conclusion, a temporal relationship (not necessarily specific) exists between increased adrenergic activity in the MBH of oestrogen-treated 22-day-old rats and a surge of gonadotrophins (LH and/or prolactin) 2 h later. This relationship apparently depends on an oestrogen-stimulated circadian rhythm of PNMT activity.

J. Endocr. (1986) 109, 45–51

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Clement K M Ho Prostate Research Group, Endocrinology Unit, Clinical Biochemistry, University of Edinburgh Cancer Research Centre, Western General Hospital, 4th floor MRC Human Genetics Building, Crewe Road South, Edinburgh EH4 2XU, UK
Prostate Research Group, Endocrinology Unit, Clinical Biochemistry, University of Edinburgh Cancer Research Centre, Western General Hospital, 4th floor MRC Human Genetics Building, Crewe Road South, Edinburgh EH4 2XU, UK

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Jyoti Nanda Prostate Research Group, Endocrinology Unit, Clinical Biochemistry, University of Edinburgh Cancer Research Centre, Western General Hospital, 4th floor MRC Human Genetics Building, Crewe Road South, Edinburgh EH4 2XU, UK

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Karen E Chapman Prostate Research Group, Endocrinology Unit, Clinical Biochemistry, University of Edinburgh Cancer Research Centre, Western General Hospital, 4th floor MRC Human Genetics Building, Crewe Road South, Edinburgh EH4 2XU, UK

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Fouad K Habib Prostate Research Group, Endocrinology Unit, Clinical Biochemistry, University of Edinburgh Cancer Research Centre, Western General Hospital, 4th floor MRC Human Genetics Building, Crewe Road South, Edinburgh EH4 2XU, UK

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Oestrogens have been implicated as a cause of benign prostatic hyperplasia (BPH). Previous animal studies led to the hypothesis that oestrogens can stimulate prostate growth, resulting in hyperplasia of the gland. In humans, the precise role of oestrogens in BPH pathogenesis is currently unclear. We investigated the direct effects of oestradiol on the proliferation of BPH-derived prostate cells in culture. Oestradiol (10−7 and 10−6 M) moderately increased the proliferation of stromal cells in culture; this stimulation was antagonised by anti-oestrogen ICI 182 780, indicating an oestrogen receptor (ER)-mediated mechanism. By contrast, oestradiol had no effects on the proliferation of epithelial cells in culture. Parameters that can determine the response of stromal cells to oestrogens, including expression of the two ER subtypes and aromatase activity, were investigated. ERβ expression in stromal cells in culture was demonstrated by immunohistochemistry and western blot analysis, and was confirmed by semi-quantitative RT-PCR showing higher expression of ERβ than ERα mRNA in stromal cells. Aromatase, the enzyme that converts androgen precursors to oestrogens, was also examined. Aromatase mRNA and activity were detected in stromal, but not epithelial cells in culture, suggesting a mechanism whereby oestrogen concentrations can be regulated in the BPH stroma. Taken together, these findings support the hypothesis that oestrogens play a role in the pathogenesis of BPH, a disease characterised predominantly by stromal overgrowth.

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