FINE STRUCTURE OF RAT PROLACTIN CELLS AFTER TREATMENT WITH A LONG ACTING DEPOT CONTRACEPTIVE

1978 ◽  
Vol 89 (2) ◽  
pp. 251-262 ◽  
Author(s):  
G. Aumüller ◽  
R. Wagner ◽  
K. J. Gräf
Keyword(s):  
Mammary Gland ◽  
Female Rats ◽  
Prolactin Cells ◽  
Stimulatory Action ◽  
Treatment Regimens ◽  
Morphological Findings ◽  
Oestradiol Benzoate ◽  
Rat Mammary Gland ◽  
Long Acting

ABSTRACT Adult intact female rats were injected with norethisterone oenanthate (NOe), with or without simultaneous administration of CB-154, or with oestradiol benzoate (OeB). The ultrastructure of prolactin (PRL) cells due to the various treatment regimens was investigated and compared with the situation found in controls. Both after treatment with NOe or NOe plus CB-154, the number of PRL cells increased and displayed various ultrastructure signs of stimulation. The determination of serum PRL levels coincides with these morphological findings. In all treated animals mammary gland DNA content was significantly increased. The results presented indicate that proliferative changes in the rat mammary gland depend predominantly on the presence of progestogenic activities additionally to PRL, whereas the effect of oestrogens was regarded as an indirect effect via their PRL-stimulatory action.

INDUCTION OF PROLACTIN AND LUTEINIZING HORMONE RELEASE BY HISTAMINE IN MALE AND FEMALE RATS AND THE INFLUENCE OF BRAIN TRANSMITTER ANTAGONISTS

1978 ◽  
Vol 76 (2) ◽  
pp. 193-202 ◽  
Author(s):  
A. O. DONOSO
Keyword(s):  
Prolactin Secretion ◽  
Oestrous Cycle ◽  
Female Rats ◽  
Male Rats ◽  
Intraventricular Injection ◽  
Hormone Release ◽  
Stimulatory Action ◽  
Male And Female Rats ◽  
Oestradiol Benzoate ◽  
Lh Release

The levels of prolactin and LH in the plasma of rats were determined at various times after intraventricular injection of histamine. Doses of 5 and 60 μg histamine (free base) in male rats, anaesthetized with ether, induced an increase in the level of prolactin in the plasma, whilst producing a slight decrease in the concentration of LH. Injection of 5 μg histamine at 14.00 h into female rats at all stages of the oestrous cycle caused prolactin to be released; the effect was greatest at oestrus and at day 1 of dioestrus. Histamine also gave rise to a marked increase in the level of LH in the plasma when administered to pro-oestrous rats, but had no effect when injected at the other stages of the oestrous cycle. The effect of histamine on the release of prolactin in ovariectomized, oestradiol benzoate: progesterone-primed (OVX,OB:P) rats was found to be dose-related, and the level of LH in the plasma was increased by as little as 1·25 μg. Pretreatment with adrenergic (phenoxybenzamine and propranolol) and cholinergic (atropine) antagonists failed to block the stimulatory effects of histamine on prolactin secretion, but pretreatment with methysergide (serotonin antagonist) increased the histamine-induced release of prolactin in male rats. Antagonists did not modify the response of prolactin to histamine in OVX,OB:P-primed rats. The histamine-induced release of LH in OVX,OB:P-primed rats was slightly reduced by pretreatment with phenoxybenzamine, propranolol and atropine, but not by methysergide. These results indicate that histamine facilitates the release of prolactin. The stimulatory action of histamine on both pro-oestrous and OVX,OB:P-primed but not male rats suggests that histamine may be involved in LH release in the rat. Results obtained in animals pretreated with transmitter antagonists, which were unable to prevent histamine-induced hormone release, suggest that the actions of this amine are not mediated by cholinergic, noradrenergic or serotonergic mechanisms.

EFFECT OF PROLACTIN INHIBITORY AGENTS ON THE ECTOPIC ANTERIOR PITUITARY AND THE MAMMARY GLAND IN RATS

1977 ◽  
Vol 85 (2) ◽  
pp. 267-278 ◽  
Author(s):  
K.-J. Gräf ◽  
R. Horowski ◽  
M. F. El Etreby
Keyword(s):  
Mammary Gland ◽  
Anterior Pituitary ◽  
Direct Action ◽  
Mammary Glands ◽  
Female Rats ◽  
Simultaneous Administration ◽  
Dopaminergic Receptors ◽  
Oestradiol Benzoate ◽  
Biological Effectiveness ◽  
Inhibitory Agents

ABSTRACT The purpose of the present study was to investigate the biological effectiveness of two highly potent prolactin (PRL) inhibitors, lisuride hydrogen maleate (LMH) and 2-Br-α-ergocryptine (CB-154), in the absence of hypothalamic factors acting directly at the level of the anterior pituitary. Hypophysectomized female rats bearing 4 transplanted pituitaries beneath the kidney capsules were treated with oestradiol benzoate (OeB) and progesterone (P) with or without simultaneous administration of LHM or CB-154 for 22 days in order stimulate or inhibit lobulo-alveolar growth of the mammary glands. In addition to the investigation of the mammary glands by DNA determination and assessment of the histological pictures, the aim of this study was directed towards the influence of the substances tested at the level of the anterior pituitary remote from the hypothalmus. In this connection the changes in the different cells within the ectopic pituitaries as revealed by immunoenzyme-cytochemical studies were investigated. The results obtained support the classical view of a neuroendocrine regulation of mammary gland growth and the importance of oestrogens, P and PRL within this system. Both ergot derivatives LHM and CB-154 were able to antagonize the stimulatory effect of OeB combined with P on the mammary gland. With regard to the mechanism of action of LHM and CB-154 it is concluded that both substances act via a direct action on dopaminergic receptors within the ectopic anterior pituitary.

CYTOCHROME OXIDASE AND SUCCINIC OXIDASE ACTIVITY IN MAMMARY GLAND MITOCHONDRIA OF LACTATING RATS

1955 ◽  
Vol 33 (1) ◽  
pp. 904-908
Author(s):  
Jules Tuba ◽  
Patricia F. Orr ◽  
G. Stuart Wiberg
Keyword(s):  
Mammary Gland ◽  
Cytochrome Oxidase ◽  
Oxidase Activity ◽  
Succinic Dehydrogenase ◽  
Female Rats ◽  
Oxidative Enzymes ◽  
Mammary Tissue ◽  
Control Group ◽  
Succinic Dehydrogenase Activity ◽  
Rat Mammary Gland

The effect of lactation on some oxidative enzymes of rat mammary gland mitochondria was examined. Cytochrome oxidase levels were nearly doubled during lactation. Succinic oxidase activity was not demonstrable in breeder female rats four days after the cessation of nursing, or in a control group (non-lactating breeder females, which had weaned their young at least four weeks previously), but during the nursing period considerable activity of the enzyme was observed. Succinic dehydrogenase activity was negligible in mitochondria during involution of rat mammary tissue. On the other hand appreciable anaerobic glycolysis occurred in the resting gland. The greatly increased metabolic activity associated with lactation is reflected in the altered behavior of some of the enzymes of rat mammary gland mitochondria.

DIRECT ACTION OF TESTOSTERONE PROPIONATE ON THE RAT MAMMARY GLAND

1962 ◽  
Vol 40 (2) ◽  
pp. 265-276 ◽  
Author(s):  
K. Ahrén ◽  
L. Hamberger
Keyword(s):  
Mammary Gland ◽  
Testosterone Propionate ◽  
Direct Action ◽  
Local Effect ◽  
Hormonal Control ◽  
Female Rats ◽  
The Third ◽  
Alveolar Development ◽  
Male And Female Rats ◽  
Rat Mammary Gland

ABSTRACT Testosterone propionate in arachis oil was applied locally to the skin over the third left thoracic mammary gland (= experimental gland) of castrated male and female rats. Arachis oil was applied to the third right thoracic mammary gland (= control gland). After 21–23 days of local applications the development of the experimental and control glands was studied on whole mount preparations. It was found that small doses of testosterone (0.15 mg daily) stimulated slight but definite lobule-alveolar development in the experimental glands, while the control glands did not show any alveoli. Applications of higher doses of testosterone propionate (0.30 and 0.75 mg daily) stimulated extensive lobule-alveolar development in the experimental glands, while only few alveoli were produced in the control glands. It may therefore be concluded that the effect of testosterone on the rat mammary gland is not mediated through other endocrine glands, but is a direct, local effect on the mammary gland structures. The result is discussed in relation to our present knowledge of the hormonal control of different growth processes within the mammary glands.

Mammary gland function and development: effect of zinc deficiency in rat

1980 ◽  
Vol 238 (1) ◽  
pp. E26-E31 ◽  
Author(s):  
P. B. Mutch ◽  
L. S. Hurley
Keyword(s):  
Mammary Gland ◽  
Zinc Deficiency ◽  
Dna Content ◽  
Late Pregnancy ◽  
Female Rats ◽  
Deficient Diet ◽  
Pregnancy And Lactation ◽  
Rat Mammary Gland ◽  
Gland Function ◽  
Zinc Deficient Diet

The effect of dietary zinc deficiency during late pregnancy and lactation on the rat mammary gland was investigated by feeding female rats either a zinc-deficient diet (0.4 ppm Zn) or a zinc-sufficient diet (100 ppm Zn) ad libitum or restricted in amount. Zinc deficiency from day 0 of lactation specifically reduced the total RNA content of lactating mammary glands on day 14, but had no effect beyond that of food restriction on their total DNA content, Both RNA and DNA content of the mammary gland were decreased by reduced food intake. Zinc deficiency from day 14 of pregnancy to day 2 of lactation severely impaired parturition and prevented the normal rise in mammary gland RNA seen during lactogenesis in control animals. A shorter deficiency period, from day 18 of gestation, had no effect on mammary gland nucleic acids other than that due to inanition.

scholarly journals Androgen Dependent Mammary Gland Virilism in Rats Given the Selective Estrogen Receptor Modulator LY2066948 Hydrochloride

2005 ◽  
Vol 33 (6) ◽  
pp. 711-719 ◽  
Author(s):  
Daniel G. Rudmann ◽  
Ilene R. Cohen ◽  
Michelle R. Robbins ◽  
David E. Coutant ◽  
Judith W. Henck
Keyword(s):  
Estrogen Receptor ◽  
Mammary Gland ◽  
Selective Estrogen Receptor Modulator ◽  
Female Rats ◽  
Male Rat ◽  
Normal Male ◽  
Female Rat ◽  
Androgen Receptor Antagonist ◽  
Receptor Modulator ◽  
Rat Mammary Gland

A selective estrogen receptor modulator (SERM) is a nonsteroidal compound with tissue specific estrogen receptor (ER) agonist or antagonist activities. In animals, SERMs may produce morphologic changes in hormonally-sensitive tissues like the mammary gland. Mammary glands from female rats given the SERM LY2066948 hydrochloride (LY2066948) for 1 month at ≥ 175 mg/kg had intralobular ducts and alveoli lined by multiple layers of vacuolated, hypertrophied epithelial cells, resembling in part the morphology of the normal male rat mammary gland. We hypothesized that these SERM-mediated changes represented an androgen-dependent virilism of the female rat mammary gland. To test this hypothesis, the androgen receptor antagonist flutamide was co-administered with LY2066948 (175 mg/kg) to female rats for 1 month. Female rats given SERM alone had hyperandrogenemia and the duct and alveolar changes described here. Flutamide cotreatment did not affect serum androgen levels but completely blocked the SERM-mediated mammary gland change. In the mouse, a species that does not have the sex-specific differences in the mammary gland observed in the rat, SERM treatment resulted in hyperandrogenemia but did not alter mammary gland morphology. These studies demonstrate that LY2066948 produces species-specific, androgen-dependent mammary gland virilism in the female rat.

Ultrastructural Description of three Different Epithelial Cell Types in Rat Mammary Gland.

1976 ◽  
Vol 34 ◽  
pp. 146-147
Author(s):  
I.H. Russo ◽  
M. Ireland ◽  
W. Isenberg ◽  
J. Russo
Keyword(s):  
Mammary Gland ◽  
Virgin Female ◽  
Cell Types ◽  
Myoepithelial Cells ◽  
Uranyl Acetate ◽  
Female Rats ◽  
Sprague Dawley ◽  
Rat Mammary Gland ◽  
Intermediate Cells ◽  
Different Cell Types

The mammary gland is composed of epithelial and myoepithelial cells. In the present work, we show that the epithelial component is composed of three types of cells differing in their ultrastructural profiles.Sprague-Dawley virgin female rats, 60 to 100 days old, were sacrificed during estrus. The mammary gland was fixed in Karnovsky's fluid (1), embedded in Epon-Araldite (2), thin-sectioned, stained with uranyl acetate and lead citrate, and examined in an Hitachi HU-11A or a Siemens Elmiskop 1A. To see whether ultrastructural differences correspond to size differences, the nuclear and cytoplasmic areas of 1000 cells were determined from photographs at 10,000X, using a compensating polar planimeter.The population of epithelial cells in the mammary gland is comprised of three different cell types (Fig. 1): a) light cells, b) dark cells, and c) intermediate cells.

CYTOCHROME OXIDASE AND SUCCINIC OXIDASE ACTIVITY IN MAMMARY GLAND MITOCHONDRIA OF LACTATING RATS

1955 ◽  
Vol 33 (6) ◽  
pp. 904-908 ◽  
Author(s):  
Jules Tuba ◽  
Patricia F. Orr ◽  
G. Stuart Wiberg
Keyword(s):  
Mammary Gland ◽  
Cytochrome Oxidase ◽  
Oxidase Activity ◽  
Succinic Dehydrogenase ◽  
Female Rats ◽  
Oxidative Enzymes ◽  
Mammary Tissue ◽  
Control Group ◽  
Succinic Dehydrogenase Activity ◽  
Rat Mammary Gland

The effect of lactation on some oxidative enzymes of rat mammary gland mitochondria was examined. Cytochrome oxidase levels were nearly doubled during lactation. Succinic oxidase activity was not demonstrable in breeder female rats four days after the cessation of nursing, or in a control group (non-lactating breeder females, which had weaned their young at least four weeks previously), but during the nursing period considerable activity of the enzyme was observed. Succinic dehydrogenase activity was negligible in mitochondria during involution of rat mammary tissue. On the other hand appreciable anaerobic glycolysis occurred in the resting gland. The greatly increased metabolic activity associated with lactation is reflected in the altered behavior of some of the enzymes of rat mammary gland mitochondria.

Anti-oestrogenic effects of tamoxifen on mammary gland and hypophysis in female rats

1984 ◽  
Vol 105 (3) ◽  
pp. 360-370 ◽  
Author(s):  
Stephan Götze ◽  
Yukishige Nishino ◽  
Friedmund Neumann
Keyword(s):  
Mammary Gland ◽  
Combined Treatment ◽  
Secretory Activity ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Immunoperoxidase Staining ◽  
Immunoperoxidase Technique ◽  
Basal Secretion ◽  
Whole Mount ◽  
Oestradiol Benzoate

Abstract. Adult ovariectomized rats were treated for 14 days with oestradiol benzoate (E2B) 15 μg/kg/d and oestradiol benzoate 15 μg/kg/d + progesterone (PRO) 15 mg/kg/d for induction of mammary gland parenchymal stimulation. Histological examination and whole mount preparation demonstrated that ductal growth in the mammary gland after E2B treatment was completely antagonized by tamoxifen (TAM) 0.5 mg/kg/d. Parallel DNA concentrations in the mammary gland were decreased to control levels by TAM 0.5, 5 and 15 mg/kg/d. E2B-induced hyperprolactinaemia in the forenoon (basal secretion was equally reduced by TAM 0.5, 5 and 15 mg/kg/d). In the afternoon, when prolactin (Prl) secretion is at its maximum, TAM 0.5 mg/kg/d turned out to be ineffective to abolish Prl surge, but TAM 5 and 15 mg/kg/d reduced serum Prl concentrations in a doserelated manner. Immunoperoxidase staining of Prl cells in the pars distalis of the hypophysis indicated that adaptive hypertrophy and signs of hypersecretion after E2B were abolished by TAM 5 mg/kg/d. Luteotrophic cells clearly showed cellular atrophy, regression and secretory inactivity. Maximal tubulo-alveolar mammary parenchymal stimulation in rats treated with E2B-PRO was slightly inhibited by TAM 0.5 mg/kg/d. Histology showed a small disseminated parenchymal islet. DNA concentrations only were partially decreased by the anti-oestrogen though serum Prl concentrations were found to be completely decreased to control levels. Secretory activity of Prl cells was reduced by TAM 0.5 mg/kg/d. In E2B-PRO treated rats lisuride had poor inhibitory activity on Prl levels and none on DNA concentrations in the mammary gland. Combined treatment with TAM and lisuride significantly decreased DNA concentration in the mammary gland compared to animals which received E2B-PRO. Also Prl levels were at a minimum. Histology performed on the mammary gland showed only slight tubulo- but no tubulo-alveolar activation. Luteotrophic cells in the pituitary gland stained by the immunoperoxidase technique appeared regressive, shrunken and atrophied.

Transcription of prolactin gene in milk secretory cells of the rat mammary gland

1993 ◽  
Vol 136 (2) ◽  
pp. 271-NP ◽  
Author(s):  
R. W. Steinmetz ◽  
A. L. Grant ◽  
P. V. Malven
Keyword(s):  
In Situ Hybridization ◽  
Mammary Gland ◽  
Female Rats ◽  
Northern Analysis ◽  
Mammary Tissue ◽  
Secretory Cells ◽  
Northern Blot Hybridization ◽  
Target Tissue ◽  
Rat Mammary Gland

ABSTRACT In-situ hybridization and Northern blot hybridization were used to identify mRNA for pituitary prolactin in mammary tissue obtained from female rats 1 day before expected parturition, 1 day after parturition and on day 7 of lactation. Prolactin cDNA was labelled with 32P for Northern analysis and with digoxigenin for in-situ hybridization. Total and poly(A)+ RNA from pituitary, mammary and control (fat and kidney) tissues were analysed by agarose gel electrophoresis with transfer to nitrocellulose and hybridization to a cDNA for rat prolactin. Although present in much smaller amounts than the 1·0 kb transcript in pituitary RNA homogenates, mammary RNA homogenates from all three stages contained mRNA of approximately 1·0 kb which hybridized with the prolactin probe. Similar analyses of fat and kidney failed to reveal any hybridization at the 1·0 kb size. When tissue sections were hybridized to the cDNA probe, specific hybridization was observed in the milk secretory cells of the mammary alveoli and the lactotroph cells of the anterior pituitary, but not in liver cells or in RNase-treated sections of mammary tissue. In summary, these results demonstrate that milk secretory cells of the rat mammary gland transcribe the gene for prolactin, and they raise the possibility that a primary target tissue for blood-borne prolactin may also synthesize prolactin. Journal of Endocrinology (1993) 136, 271–276

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