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T. J. HAYDEN
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S. V. SMITH
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The response of. prolactin receptor and lactose synthetase to suppression of plasma concentrations of prolactin was examined in normal and occluded (teat-sealed) mammary glands of Sprague–Dawley rats. Rats, with mammary glands unilaterally occluded, were given bromocriptine (2·5 mg/kg per 12 h) between days 5 and 8 post partum. Bromocriptine reduced plasma prolactin concentrations from 460·4±120·8 (mean ±s.e.m.) to 2·56 ± 0·89 ng/ml within 12 h whilst concentrations in control rats were 553·4± 110·25 ng/ml. Lactose synthetase activity declined rapidly, within 24 h, in occluded glands of both groups but was maintained for 24 h in normal glands of bromocriptine-treated rats and decreased thereafter. Prolactin receptors also declined significantly within 24 h in occluded glands. Desaturation of the prolactin receptor by bromocriptine treatment in vivo was compared with desaturation by exposure of membranes to MgCl2 in vitro. Both treatments enhanced prolactin binding but the increase after treatment with MgCl2 may have been partly artefactual since there was a selective loss of protein from the membranes. These results indicate that the prolactin receptor in rat mammary gland may be maintained after acute suppression of prolactin secretion.

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T. J. HAYDEN
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ROSEMARY C. BONNEY
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ISABEL A. FORSYTH
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Prolactin receptors were identified and partially characterized in the mammary gland of the rat. The binding of 125I-labelled ovine prolactin to a subcellular particulate fraction of rat mammary gland decreased between days 30 and 100 of age. Over the same period, binding to the liver increased and there was a significant negative correlation between prolactin binding in the two tissues. Binding to the mammary gland was low during pregnancy, increased in early lactation and declined after the litters were weaned. Binding to the liver was lower during lactation than during pregnancy or the period after weaning suggesting that tissue-specific factors may operate in the control of this receptor. In virgin rats, prolactin binding by the mammary gland was increased by oestrogen. This effect was blocked by hypophysectomy and partially restored by replacement therapy with prolactin. Hypothyroidism and treatment with progesterone also reduced the response to oestrogen. The maintenance of prolactin binding by the mammary gland of lactating rats depends on the presence of the ovaries and pituitary, thyroid and adrenal glands. Examination of the ratio epithelium: stroma suggests that prolactin acts by increasing the number of epithelial cells in the mammary gland and that thyroid, adrenal and ovarian hormones modulate the number of receptors per cell.

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T. J. HAYDEN
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C. R. THOMAS
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SUSAN V. SMITH
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ISABEL A. FORSYTH
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Placental lactogen has been measured in goats throughout pregnancy by radioreceptor assay of prolactin-like activity. Lactogenic activity, which is not prolactin, increased from less than 5 nmol/l in week 8 to 27 nmol/l by week 16. There was no further change until term. Plateau concentrations (week 16 to term) were highest in animals carrying triplets, 49·5 nmol/l. There were marked fluctuations in placental lactogen over a 24 h period. These short-term fluctuations were not related to changes in glucose, non-esterified fatty acids or, in two animals, progesterone. However, there was a negative correlation between mean concentrations of placental lactogen and glucose in plasma of 20 goats sampled over a 24 h period between weeks 15 and 20 of gestation. There was no difference in placental lactogen concentration from week 16 to term between goats in their first and second pregnancies although the normal period of increase in placental lactogen was delayed by some 3 weeks in goats in their second pregnancy. In hemimastectomized goats, hypophysectomy on day 60 did not affect placental lactogen but daily treatment with bromocriptine (5 mg/day) from day 60 to day 120 blocked the normal rise in concentration.

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