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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 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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Department of Applied Pharmacology, School of Pharmacy, The Hebrew University, Jerusalem, Israel
(Received 30 January 1976)
Fluctuations in serum prolactin levels after treatment with tranquillizers led to the recognition of a 'biphasic effect' in prolactin release. A double peak in the hormone level occurs after treatment, the first immediately and the second a few days later. It appears from previous work utilizing labelled haloperidol and perphenazine (Shani, Ziv, Givant, Buchman & Sulman, 1974; Ziv, Shani, Givant, Buchman & Sulman, 1974) that these two tranquillizers exert their biphasic effect through binding to serum proteins, from which they are released in wave form.
Regarding mammotrophic development after tranquillizers, Arai & Suzuki (1971) demonstrated a biphasic response in male rat mammary glands after a single injection of reserpine, with a rapid phase around day 2 and a prolonged phase between days 8 and 12. McNeilly & Lamming (1971) mention a biphasic prolactin peak
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The effects of prolactin on various tissues have been reviewed recently by Sulman (1970). In the search for target receptors of prolactin, the capacities of pigeon crop sac mucosa and of the rat mammary gland to bind labelled prolactin were investigated. Cox (1951) used labelled prolactin for similar studies in mice and found appreciable amounts of radioactivity in the mammary glands but noticed rapid breakdown of the labelled hormone.
For the present study two methods were used: (a) radioactivity was measured in mammary glands of lactating rat mothers 1–12 h after i.v. injection of 125I-labelled prolactin; (b) mucosal proliferation and uptake of radioactivity by the pigeon crop were measured after local injection of 125I-labelled prolactin, 125I-labelled human chorionic gonadotrophin (HCG), 131I-labelled albumin or Na125I. Iodination was carried out according to Greenwood, Hunter & Glover (1963), using Na125I (Amersham) and PS-9 prolactin (N.I.H.)
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Department of Applied Pharmacology, School of Pharmacy, Hebrew University of Jerusalem, *Institute of Endocrinology, The Chaim Sheba Medical Center, Tel-Hashomer, Ramet-Gan, and Department of Life Sciences, Bar-Ilan University, Ramat-Gan, Israel
(Received 25 November 1975)
There is evidence that cyclic AMP mediates the secretion of adenohypophysial hormones induced by hypothalamic releasing hormones (Labrie, Pelletier, Lemay, Borgeat & Burden, 1973), that mammary gland explants respond to prolactin with increased levels of cyclic AMP (Scott & Howard, 1975), and that prolactin enhances adenyl cyclase activity when incubated with prostate homogenate (Golder, 1972). We therefore decided to examine the possible role of cyclic AMP in a local and highly specific effect: mediating stimulation of the pigeon crop sac by prolactin. Using this model it had already been demonstrated that ATP or GTP, but not cyclic AMP, potentiates the stimulatory effect of prolactin on proliferation of the pigeon crop sac (Sinha & Schmidt, 1970).
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