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P. MacKinnon, C. Clark, E. M. Clement, and R. Sheaves


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, P. C. B. MacKinnon, and R. Sheaves


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 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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N Delorme, C Remond, H Sartelet, E Petitfrere, C Clement, C Schneider, G Bellon, A Virion, B Haye, and L Martiny

Thyrotropin (TSH) and transforming growth factor beta 1 (TGFbeta1) have major roles in the regulation of folliculogenesis and differentiation in thyroid cells. Isolated porcine thyroid cells cultured in the presence of TSH on a plastic surface recover a follicular architecture and exhibit normal functional properties. The addition of TGFbeta1 to the culture medium induces important morphological changes and extracellular matrix remodelling. Similarly, thyroid cells lose their ability to organify iodine and their responsiveness to adenylate cyclase. The aim of this study was to analyse the influence of TGFbeta1 on the functional activity of thyrocytes in suspension culture, independent of follicle disruption. In this system, we demonstrate that TGFbeta1 inhibits expression of thyroperoxidase, NADPH oxidase activity, iodine uptake and, consequently, iodine organification. Moreover, TGFbeta1 decreases basal and TSH-stimulated cAMP production and TSH receptor expression. Taken together, these data converge to demonstrate an essential role of TGFbeta1 in the regulation of the thyroid cell function.