The stimulated C-kinase activity in estradiol-treated rat pituitaries is reduced by chronic treatment with the dopamine agonist CV 205-502

1989 ◽  
Vol 121 (4) ◽  
pp. 489-494 ◽  
Author(s):  
P. Birman ◽  
Ph. Touraine ◽  
F. Bai-Grenier ◽  
C. Dubray ◽  
T. Kaabache ◽  
...  
Keyword(s):  
Dopamine Agonist ◽  
Kinase Activity ◽  
Soluble Fraction ◽  
Prolactin Secretion ◽  
Cell Multiplication ◽  
Estradiol Treatment ◽  
Pituitary Glands ◽  
Estradiol Stimulation ◽  
Plasma Prl ◽  
Stimulation Of

Abstract. To investigate whether the modulation of lactotrope cell multiplication and prolactin secretion in rat pituitary glands implicated the phosphoinositide C-kinase system, female Wistar rats were treated or not with the dopamine agonist CV 205-502 or 8 days or with estradiol cervical implants for 8 for 15 days, alone or in combination with CV 205-502 for the last 8 days. CV 205-502 treatment induced a significant reduction in plasma PRL levels and in pituitary weights, whereas estradiol treatment induced a significant increase in both parameters. CV 205-502, in association with estradiol, counteracted estradiol stimulation of PRL levels and of pituitary weights. Total C-kinase activity in controls was 29.8 ± 9.9 pmol 32phosphorus/min (N = 7, mean±sem), mainly found in the soluble fraction (84%). When administered alone, CV 205-502 induced a significant reduction (–58%, p < 0.02) in C-kinase activity in the particulate fraction with no modification in the soluble fraction. Both 8 and 15 days estradiol treatment induced a significant stimulation of total C-kinase activity, 74% and 155% respectively. When combined with estradiol, CV 205-502 significantly (p < 0.02) counteracted the estradiol increase in total C-kinase activity, which was only 45% over control values. We conclude that treatment with a dopamine agonist and estradiol, which have antagonistic effects on the pituitary, exerts an opposite regulation of C-kinase activity. Whether this may be one of the mechanisms involved in their interaction on pituitary lactotropes remains to be determined.

The dopaminergic regulation of anterior pituitary 45Ca2+ homeostasis and prolactin secretion

1986 ◽  
Vol 108 (3) ◽  
pp. 423-429 ◽  
Author(s):  
M. P. Schrey ◽  
H. J. Clark ◽  
S. Franks
Keyword(s):  
Dopamine Agonist ◽  
Anterior Pituitary ◽  
Prolactin Secretion ◽  
Prolactin Release ◽  
Pituitary Glands ◽  
Dopaminergic Regulation ◽  
Cellular Ca ◽  
Stimulation Of ◽  
Dopaminergic Control

ABSTRACT A role for the regulation of cellular Ca2+ homeostasis in the dopaminergic control of prolactin secretion was investigated in rat anterior pituitary glands. Withdrawal of dopamine stimulated the uptake of 45Ca2+ into hemipituitary tissue by 48% after 3 min. Radioisotope desaturation from tissue prelabelled with 45Ca2+ was significantly retarded in the presence of dopamine. Withdrawal of dopamine rapidly stimulated 45Ca2+ efflux from prelabelled tissue by 79% and was accompanied by a three- to fourfold rise in prolactin secretion. The 45Ca2+ efflux response to dopamine withdrawal was reduced in tissue prelabelled in the presence of dopamine. Agonist displacement with metoclopramide mimicked the effect of dopamine withdrawal on 45Ca2+ efflux and prolactin secretion. These observations demonstrate that the stimulation of prolactin release by dopamine withdrawal is accompanied by a redistribution of cellular Ca2+ and support the hypothesis that dopamine inhibits secretion by decreasing Ca2+ influx in the mammotroph cell. J. Endocr. (1986) 108, 423–429

Estradiol stimulation of prolactin secretion in horses: Interaction with type of secretagogue

2011 ◽  
Vol 31 (5-6) ◽  
pp. 308
Author(s):  
D.L. Thompson ◽  
S.E. Clavier ◽  
P.B. Mitcham ◽  
L.R. Earl
Keyword(s):  
Prolactin Secretion ◽  
Estradiol Stimulation ◽  
Stimulation Of

Influence of lactotroph cell density on prolactin secretion in rats

1992 ◽  
Vol 134 (2) ◽  
pp. 241-NP ◽  
Author(s):  
H. A. Pasolli ◽  
A. I. Torres ◽  
A. Aoki
Keyword(s):  
Volume Density ◽  
Experimental Models ◽  
Prolactin Secretion ◽  
Morphological Data ◽  
Ovariectomized Rats ◽  
Molecular Forms ◽  
Serum Prolactin ◽  
Pituitary Glands ◽  
Prolactin Content ◽  
Stimulation Of

ABSTRACT The relationships between the stimulation of prolactin secretion and proliferation of lactotrophs was studied from a multidisciplinary standpoint in three experimental models. Administration of both oestrogen and sulpiride resulted in a significant increase in prolactin secretion and in the lactotroph population. A single injection of 10 μg oestradiol benzoate (OB) induced a twofold increase in the proliferation of lactotrophs (morphometrically as volume density), which increased further (2·5-fold) after three OB injections. Parallel changes were observed in the net counts made on lactotrophs sectioned through the nucleus to avoid possible distortions in volume density caused by hypertrophic cytoplasms. Comparable results were obtained with the mitotic index in the same groups of rats exposed to treatment with colchicine. The effect of sulpiride on proliferation of lactotrophs was also significant (1·7-fold) but less pronounced than in rats treated with oestrogens. The treatments with oestrogen and sulpiride did not stimulate lactotrophic activity in a similar way, as judged by the levels of serum prolactin and the storage patterns of small and big prolactin in pituitary glands. Serum prolactin (mean ± s.e.m.) in control ovariectomized rats was 4·0±0·9 μg/l and one and three injections of OB raised these levels to 14·4±5·0 and 28·8±4·6 μg/l respectively. The highest levels of serum prolactin were seen in sulpiride-treated rats (467·2±28·7 μg/l). Striking differences occurred in the pituitary contents of big prolactin, the control values increasing from 5·3±0·5 to 10·2±1·3 μg/mg after one OB injection and to 14· 7 ±0·7 μg/mg after three OB injections. In contrast, the concentration of big prolactin in sulpiride-treated rats was very low (1·85 ± 0·2 μg/mg), 2·8-times smaller than the controls. Other changes were also found in the small prolactin content in pituitary tissue with higher values in all the experimental models. These differences could only be detected after differential extraction of big and small molecular forms of prolactin. In ovariectomized rats, treatment with several doses of oestrogen enhanced the proliferation observed in the lactotroph population and increased the number of mitoses. In turn, morphological data could be closely related to the higher levels of prolactin in serum and pituitary glands. A sustained stimulation of lactotrophic secretion was always followed by proliferation of lactotrophs, the number of which fluctuated in parallel with the degree of stimulation. Journal of Endocrinology (1992) 134, 241–246

Inhibition by testosterone of prolactin and growth hormone release from chicken anterior pituitary glands in vitro

1984 ◽  
Vol 102 (2) ◽  
pp. 153-159 ◽  
Author(s):  
T. R. Hall ◽  
S. Harvey ◽  
A. Chadwick
Keyword(s):  
Anterior Pituitary ◽  
Prolactin Secretion ◽  
Prostaglandin E ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Prolactin Release ◽  
Thyrotrophin Releasing Hormone ◽  
Pituitary Glands ◽  
Stimulation Of

ABSTRACT Pituitary glands and hypothalami from broiler fowl were incubated in medium containing testosterone, and prolactin and GH release were determined. Pituitary glands were also preincubated for 20 h in medium containing testosterone, and then in medium containing various secretagogues. Testosterone inhibited the release of prolactin directly from the pituitary gland in a concentration-related manner. The hypothalamus stimulated the release of prolactin, but by a lesser amount in the presence of testosterone. When pituitary glands were preincubated with testosterone, subsequent release of prolactin was inhibited, except with the highest concentration which stimulated prolactin release. Hypothalamic extract (HE) markedly stimulated prolactin release from control pituitary glands although testosterone-primed glands were less responsive. The stimulation of prolactin release by thyrotrophin releasing hormone (TRH) and prostaglandin E2 (PGE2) was also reduced by preincubation of the pituitary glands with testosterone. Priming with testosterone did not affect the release of GH from pituitary glands alone, but reduced the TRH-, HE- and PGE2-stimulated release of GH. These results demonstrate that testosterone directly inhibits prolactin secretion and reduces the sensitivity of pituitary lactotrophs and somatotrophs to provocative stimuli. J. Endocr. (1984) 102, 153–159

Stimulation of prolactin secretion by oestradiol in the rat is associated with increased hypothalamic release of thyrotrophin-releasing hormone

1984 ◽  
Vol 103 (2) ◽  
pp. 257-261 ◽  
Author(s):  
S. Franks ◽  
H. D. Mason ◽  
K. I. J. Shennan ◽  
M. C. Sheppard
Keyword(s):  
Incubation Medium ◽  
Prolactin Secretion ◽  
Serum Prolactin ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Threefold Increase ◽  
Rat Pituitary ◽  
Pituitary Glands ◽  
Pituitary Prolactin ◽  
Stimulation Of

ABSTRACT We have studied the effect of oestradiol (OE2) on secretion of prolactin and TSH by rat pituitary glands and correlated this with changes in hypothalamic content and release of thyrotrophin-releasing hormone (TRH). Ovariectomized Wistar rats received s.c. silicone elastomer implants of OE2 at a dose known to give pro-oestrous OE2 levels. After 1 week rats were decapitated, blood was collected for assay of prolactin and TSH, blocks of hypothalamus were dissected out and pituitary glands were removed and bisected. Medium bathing hemipituitary glands was collected for measurement of prolactin and TSH after a 30-min incubation. Immunoreactive TRH was measured in medium removed from hypothalami and in extracts of homogenized hypothalami. Serum prolactin was higher in OE2-treated than in control animals (59·3 ± 19·5 (s.e.m.) vs 9·4 ± 1·5 μg/l; P<0·05) and this was associated with a threefold increase in pituitary prolactin in the medium. By contrast, TSH concentrations in serum and pituitary incubation medium were not significantly different in the two groups. There was no difference between the groups in hypothalamic content of TRH but TRH release in the incubation medium was increased by OE2 (30·2 ± 6·5 vs 10·0 ± 1·3 pg/mg protein per 30 min; P<0·01). In summary, physiological levels of OE2 stimulated prolactin secretion without change in TSH and this was associated with a threefold increase in hypothalamic release of TRH. These findings suggest that the stimulating effect of OE2 on prolactin secretion may, in part, be mediated by hypothalamic TRH. J. Endocr. (1984) 103, 257–261

Melatonin Modulates Lactation by Regulating Prolactin Secretion Via Tuberoinfundibular Dopaminergic Neurons in the Hypothalamus- Pituitary System

2020 ◽  
Vol 21 (8) ◽  
pp. 744-750 ◽  
Author(s):  
Hongyang Li ◽  
JingyaWei ◽  
Fengtao Ma ◽  
Qiang Shan ◽  
Duo Gao ◽  
...  
Keyword(s):  
Pineal Gland ◽  
Pituitary Gland ◽  
Antioxidant Capacity ◽  
Dopaminergic Neurons ◽  
Growth And Development ◽  
Endocrine System ◽  
Mammary Glands ◽  
Prolactin Secretion ◽  
The Body ◽  
Stimulation Of

In-depth studies have identified many hormones important for controlling mammary growth and maintaining lactation. One of these is melatonin, which is synthesized and secreted by the pineal gland to regulate circadian rhythms, improve antioxidant capacity, and enhance immunity. Prolactin is secreted by the pituitary gland and is associated with the growth and development of mammary glands as well as initiation and maintenance of lactation. The hypothalamus-pituitary system, the most important endocrine system in the body, regulates prolactin secretion mainly through dopamine released from tuberoinfundibular dopaminergic neurons. This review provides a reference for further study and describes the regulation of lactation and prolactin secretion by melatonin, primarily via the protection and stimulation of tuberoinfundibular dopaminergic neurons.

scholarly journals Reconstitution of cargo-induced LC3 lipidation in mammalian selective autophagy

2021 ◽  
Vol 7 (17) ◽  
pp. eabg4922
Author(s):  
Chunmei Chang ◽  
Xiaoshan Shi ◽  
Liv E. Jensen ◽  
Adam L. Yokom ◽  
Dorotea Fracchiolla ◽  
...  
Keyword(s):  
Complex I ◽  
Kinase Activity ◽  
Protein Aggregates ◽  
Class Iii ◽  
Phosphatidylinositol 3 Kinase ◽  
Giant Unilamellar Vesicles ◽  
Core Complex ◽  
Selective Autophagy ◽  
The Core ◽  
Stimulation Of

Selective autophagy of damaged mitochondria, protein aggregates, and other cargoes is essential for health. Cargo initiates phagophore biogenesis, which entails the conjugation of LC3 to phosphatidylethanolamine. Current models suggest that clustered ubiquitin chains on a cargo trigger a cascade from autophagic cargo receptors through the core complexes ULK1 and class III phosphatidylinositol 3-kinase complex I, WIPI2, and the ATG7, ATG3, and ATG12ATG5-ATG16L1 machinery of LC3 lipidation. This was tested using giant unilamellar vesicles (GUVs), GST-Ub4 as a model cargo, the cargo receptors NDP52, TAX1BP1, and OPTN, and the autophagy core complexes. All three cargo receptors potently stimulated LC3 lipidation on GUVs. NDP52- and TAX1BP1-induced LC3 lipidation required all components, but not ULK1 kinase activity. However, OPTN bypassed the ULK1 requirement. Thus, cargo-dependent stimulation of LC3 lipidation is common to multiple autophagic cargo receptors, yet the details of core complex engagement vary between the different receptors.

scholarly journals Biosynthesis of growth hormone in the rat anterior pituitary gland. Stimulation of biosynthesis in vitro by insulin

1973 ◽  
Vol 134 (4) ◽  
pp. 1103-1113 ◽  
Author(s):  
A. Betteridge ◽  
M. Wallis
Keyword(s):  
Growth Hormone ◽  
Anterior Pituitary ◽  
Rna Synthesis ◽  
Glucose Utilization ◽  
Actinomycin D ◽  
Hormone Synthesis ◽  
Pituitary Glands ◽  
Hormone Biosynthesis ◽  
Stimulation Of

The effect of insulin on the incorporation of radioactive leucine into growth hormone was investigated by using rat anterior pituitary glands incubated in vitro. A 50% stimulation over control values was observed at insulin concentrations above 2μm (280munits/ml). The effect was specific for growth hormone biosynthesis, over the range 1–5μm-insulin (140–700munits/ml). Lower more physiological concentrations had no significant effect in this system. Above 10μm (1.4 units/ml) total protein synthesis was also increased. The stimulation of growth hormone synthesis could be partially blocked by the addition of actinomycin D, suggesting that RNA synthesis was involved. Insulin was found to stimulate the rate of glucose utilization in a similar way to growth hormone synthesis. 2-Deoxyglucose and phloridzin, which both prevented insulin from stimulating glucose utilization, also prevented the effect of insulin on growth hormone synthesis. If glucose was replaced by fructose in the medium, the effect of insulin on growth hormone synthesis was decreased. We conclude that the rate of utilization of glucose may be an important step in mediating the effect of insulin on growth hormone synthesis.

scholarly journals Proceedings: Chlorpromazine stimulation of prolactin secretion: a test of pituitary function

1974 ◽  
Vol 29 (1) ◽  
pp. 97-97 ◽  
Author(s):  
R G Wilson ◽  
B N Cole ◽  
A R Boyns ◽  
A P Forrest
Keyword(s):  
Prolactin Secretion ◽  
Pituitary Function ◽  
Stimulation Of
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