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Department of Applied Pharmacology, School of Pharmacy, The Hebrew University, Jerusalem, Israel
(Received 16 June 1976)
Existence of human prolactin (hPRL) in semen, serum and urine has been established in men and women during various physiological and endocrinopathological states (Lyons & Page, 1935; Meites & Turner, 1941; Coppedge & Segaloff, 1951; Segaloff, 1953; Sheth, Mugatwala, Shah & Rao, 1975). Recently a radioimmunological method utilizing NIH hPRL-VLS-2 for iodination and prolactin 72/4/9 as a standard preparation was described: Nader, Mashiter & Joplin (1975) and Sheth et al. (1975) reported that the level of hPRL in semen is four- to sevenfold higher than in serum as assayed in various systems. Due to the low sensitivity of these methods the urine samples had to be pretreated in order to concentrate the hormone, and it occurred to us that developing a sensitive assay method that will enable a simple and direct determination of urinary
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Department of Applied Pharmacology, School of Pharmacy, The Hebrew University, Jerusalem, Israel
(Received 9 August 1976)
Although the proliferation of the pigeon crop-sac induced by prolactin has been used during four decades for quantitative evaluation of the hormone, little is known of the molecular mechanism of this process. The crop-sac comprises layers of mucosa, sub-mucosa, muscle and skin: prolactin is known to stimulate the hyperplastic multiplication of the mucosa itself. This mucosal epithelium is a multilayer (stratified) of flat (squamous) non-cornified tissue in which cuboidal cells of the basal layer can be easily distinguished. This progressive flattening of the cells in the more superficial layers suggests that the reproductive layer is nearer the basal layer. How does prolactin stimulate this proliferation?
Previous studies from this Department have demonstrated the biological activity of 125I-labelled prolactin on the pigeon crop mucosa in vivo (Shani, Givant, Sulman, Eshkol & Lunenfeld, 1972) and in
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Perphenazine in doses of 10–50 mg kg−1 day−1 given at the early stages of pregnancy delayed nidation up to day 8 of pregnancy. Once nidation had occurred the length of the rest of the gestation period was normal. Doses of up to 20 mg perphenazine kg−1 day−1, injected on days 1–7, prolonged gestation but the mothers and young were apparently normal; lower doses were effective only when treatment commenced soon after copulation. The delay in implantation of the ovum caused by perphenazine was corrected and implantation was brought about immediately, by injection of 0·1 μg oestradiol together with perphenazine. It is suggested that perphenazine delays and prevents implantation in rats by counteracting oestrogen release from the ovaries.
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The effect of hormonal manipulations on prolactin binding to its specific binding sites in the seminal vesicle, prostate gland, testis and liver of adult male rats was studied. Castration significantly reduced prolactin binding to the seminal vesicle and prostate, whereas it greatly increased its binding to the liver. Testosterone replacement therapy restored the reduced level of binding to that found in the liver of intact rats, whereas binding to the seminal vesicle and the prostate was raised to the high levels found in the testosterone-treated intact rats. In contrast, testosterone administration to intact rats significantly reduced the binding of prolactin to the testicular homogenate. The administration of 2-bromo-α-ergocryptine (CB 154) to either intact or testosterone-treated castrated rats caused no significant change in binding of prolactin to any of the organs tested. Fluphenazine enanthate or CB 154 +ovine prolactin increased the binding of prolactin to the liver, when compared with untreated rats, whereas in the testis these treatments resulted in a minor decrease as compared with untreated rats. In the testosterone-treated castrated rats, fluphenazine caused no apparent effect on the binding of prolactin to any of the organs tested. In conclusion, testosterone is essential for the maintenance of prolactin binding sites in the seminal vesicle and prostate of the adult rat. Prolactin, however, does not appear to regulate its own receptor in the accessory sex glands, neither alone nor in synergism with testosterone. In the testis, exogenous testosterone exerted a negative effect on prolactin binding, as did raised serum prolactin levels. In the liver of the male rat, testosterone seemed to be the major cause of the low level of prolactin binding sites, while prolactin was capable of inducing its own sites in that organ.
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Faculty of Agriculture, Nagoya University, Nagoya 464, Japan
(Received 6 July 1976)
In 1965, Shinde, Ôta & Yokoyama reported that the initiation of lactose synthesis in the mammary gland could be advanced by ovariectomy and/or foeto-placentectomy performed on days 18 or 19 of pregnancy in the rat. The present experiments were designed to determine the stage of pregnancy at which the mammary gland was able to initiate lactose synthesis in response to ovariectomy. Corticosterone in plasma was also measured in relation to the changes around the time of lactogenesis reported previously (Ôta, Ôta & Yokoyama, 1974).
Primigravid Wistar-Imamichi strain rats, weighing between 200 and 280 g, were kept in a temperature- (23 ± 2°C) and light- (14h light: 10h darkness, lights on 05.00h) controlled animal room. The day on which sperm in the vagina or vaginal plugs were found was designated day 0 of pregnancy. Ovariectomy was performed between 17.30 and 18.00
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SUMMARY
The effect of 5α-androstane-3α,17β-diol, its 3β epimer and oestradiol benzoate on suppression of LH release after ovariectomy was studied in immature rats. At doses of 50 and 100 μg/100 g body weight/day the 3α compound suppressed LH release after ovariectomy to the same extent as 0·1 μg oestradiol benzoate/100 g/day. 3α-Androstanediol at a dose of 25 μg/100 g/day suppressed LH release only up to day 45 of life, while the same dose of the 3β epimer had no effect on LH suppression. The effect of 3β-androstanediol on inducing precocious vaginal opening was found to be mediated by the ovaries, since it was eliminated by ovariectomy. These results confirm our previous findings on the participation of androstanediol in the normal regulation of LH and in the mechanism of onset of puberty in the rat.
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SUMMARY
Levels of prolactin and LH were determined in serum and pituitary during the last days of pregnancy and post partum in rats bearing single and multiple embryos. In rats with a single embryo serum prolactin and LH levels were significantly lower during the last 2 days of pregnancy and post partum than in rats bearing multiple embryos. While large increases were recorded in serum prolactin and LH levels in the rats with multiple embryos between days 21 and 22 of gestation, in the group with single embryos changes occurred in LH level only. Throughout the experiment pituitary prolactin was lower in rats with a single embryo than in those with multiple embryos in spite of the sharp drop in prolactin level in the group with multiple embryos from day 21 to 22. No differences were observed in the pituitary LH levels of either group during the days preceding parturition, but in the rats with multiple embryos there was a sharp drop in LH level post partum. It seems that the reduced serum prolactin level in the rats with a single embryo was associated with inhibition of pituitary prolactin synthesis and release, whereas the decreased serum LH level resulted from impaired release but not synthesis. These results support the hypothesis of a regulatory role for the placenta in pituitary prolactin and LH synthesis and release, either by hypothalamus– pituitary stimulation, or perhaps by way of the ovaries, through regulation of ovarian steroid production.
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The capacity of the pigeon pituitary gland to release prolactin was investigated in vivo, to evaluate its hypothalamic regulation and to establish the dominant hypothalamic factor for prolactin secretion. After 3 days of systemic administration of some physiological and pharmacological agents, followed by 2 consecutive days of local intradermal injections of prolactin into their crop sacs, the crop mucosa was scraped, dried and weighed. The substances tested were: oestradiol and tamoxifen (antioestrogen), thyrotrophin-releasing hormone (TRH) and anti-TRH serum, perphenazine (releases prolactin in mammals) and bromocriptine (suppresses prolactin in mammals). Prolactin and anti-prolactin serum were tested as controls.
While prolactin markedly proliferated and anti-prolactin serum significantly inhibited the mucosal weight, oestradiol, TRH and perphenazine dramatically depressed proliferation of the mucosa, suggesting that prolactin secretion was inhibited. Tamoxifen, anti-TRH serum and bromocriptine significantly increased the proliferation of the crop mucosa, indicating an increase in the endogenous release of prolactin. Since the effect of these substances on prolactin release in the pigeon is the opposite from their well-established effects in mammals, these results suggest, in a specific and homologous model, that the dominating regulator for prolactin in the pigeon is contrary to that in the mammal, namely prolactin-releasing factor, and that TRH may play a significant role in the physiological regulation of prolactin secretion.
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The binding of ovine prolactin to the seminal vesicles of the rat has been characterized and found to be a saturable process, dependent upon time, temperature, protein concentration of the seminal vesicle and divalent ions. Its specificity was similar to that reported for prolactin binding to other organ preparations. Time and temperature studies of the specific binding revealed that equilibrium was reached after 16 h at 5 °C or 4 h at 19 °C. Non-specific binding was also dependent on time and temperature. This parameter has been reported to comprise up to 70% of the total binding to various organ-binding sites, but it fell to below 20% after 48 h at 19 °C, thus demonstrating the high degree of specificity required of target organ receptors.
From degradation studies it was evident that no damage occurred to the free hormone during incubation for up to 70 h at 5 °C or 16 h at 19 °C. However, there seems to be a difference in the susceptibility of bound and free ovine prolactin to damage during incubation: after 40 h at 19 °C the hormone in the supernatant fraction had lost 85% of its binding ability, whereas a high level of specific binding was evident in the pellet. A Scatchard plot of competitive binding studies revealed two classes of binding sites, of which the high-affinity, low-capacity site was similar to that reported previously and consistent with a physiological receptor for prolactin in the seminal vesicle of the rat.
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In view of the possible involvement of catecholamines in prolactin release, and hence in lactation, four biogenic compounds, L-noradrenaline bitartrate (Sigma), dopamine HC1 (Sigma), 5-hydroxytryptamine creatinine sulphate (5-HT) (May & Baker) and melatonin (Upjohn) were tested for their effect on the yield and composition of milk in the New Zealand White rabbit. Twenty-two lactating rabbits were used. The young were separated from their mothers on the 7th day of lactation and their number adjusted to between six and eight. Litters were allowed to suckle once each morning after their mothers had received 0·5 i.u. oxytocin i.v., and daily milk yield was calculated from the difference in weight of the litter before and after suckling. On the 9th day of lactation rabbits were anaesthetized with pentobarbitone sodium B.P. i.v., and under aseptic conditions a permanent stainless steel cannula was implanted into the brain so that the tip lay in the median
