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

ONSET OF OESTROGEN-INDUCED PROLACTIN SECRETION AND DNA SYNTHESIS BY THE RAT PITUITARY GLAND

1977 ◽  
Vol 72 (1) ◽  
pp. 35-39 ◽  
Author(s):  
JOAN JACOBI ◽  
H. M. LLOYD ◽  
J. D. MEARES
Keyword(s):  
Dna Synthesis ◽  
Pituitary Gland ◽  
Prolactin Secretion ◽  
Male Rat ◽  
Serum Prolactin ◽  
Rat Pituitary ◽  
The Times ◽  
Pituitary Prolactin

SUMMARY The times of onset of oestrogen-induced prolactin secretion and DNA synthesis were studied in the pituitary gland of the male rat. At intervals from 3 to 96 h after injection of 10 mg diethylstilboestrol dipropionate, serum and pituitary prolactin concentrations were measured by radioimmunoassay and pituitary DNA synthesis by incorporation of [3H]thymidine in vitro. Serum prolactin was raised significantly from 6 h onwards and DNA synthesis was increased from 30 h onwards. Pituitary prolactin concentration began to increase at 30 h. Significant correlations were obtained between serum prolactin and DNA synthesis from 24 to 72 h but not during the period of prolactin secretion from 6 to 24 h.

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

THE STIMULATION OF PROLACTIN SECRETION BY SULPIRIDE IN "ADOLESCENT GYNAECOMASTIA"

1977 ◽  
Vol 85 (4) ◽  
pp. 692-697
Author(s):  
R. D'Agata ◽  
S. Andó ◽  
S. Gulizia ◽  
L. Condorelli ◽  
C. Paci ◽  
...  
Keyword(s):  
Baseline Level ◽  
Prolactin Secretion ◽  
Serum Prolactin ◽  
Maximum Increase ◽  
The Mean ◽  
Pituitary Prolactin ◽  
Stimulation Of

ABSTRACT In order to evaluate the function of the hypothalamic-pituitary-prolactin axis in "adolescent gynaecomastia" (AG), sulpiride was administered to 7 normal boys and 7 boys with AG. The maximum increase in serum prolactin (PRL) above the mean baseline level (Δmax) was used as index of response. The sulpiride induced a greater PRL release in boys with gynaecomastia than in the controls. Our data indicate that boys with gynaecomastia may have a greater pituitary prolactin pool. The results also illustrate the usefulness of specific neurotrophic agents such as sulpiride as important tools for evaluating the function of the hypothalamic-pituitary-PRL axis.

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

Desensitization of rat anterior pituitary gland to thyrotrophin releasing hormone

1984 ◽  
Vol 101 (1) ◽  
pp. 101-105 ◽  
Author(s):  
M. C. Sheppard ◽  
K. I. J. Shennan
Keyword(s):  
Anterior Pituitary ◽  
Prolactin Secretion ◽  
Normal Medium ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Pituitary Tissue ◽  
Subsequent Response ◽  
Pituitary Glands ◽  
Prolactin Response

ABSTRACT We have studied the secretion of TSH and prolactin from perifused rat anterior pituitary glands in vitro in response to single pulses of thyrotrophin releasing hormone (TRH) and KCl after prior exposure to TRH. Anterior pituitary fragments were incubated in normal medium or in medium containing 28 nmol TRH/1 for 20 h before perifusion. Thyrotrophin releasing hormone (28 nmol/l), administered as a 3-min pulse, stimulated TSH and prolactin release from control tissue to a peak value four or five times that of basal. After exposure of the pituitary tissue to TRH for 20 h, the subsequent response of TSH to a 3-min pulse of TRH was, however, markedly reduced; in contrast, the prolactin response was not significantly reduced. In a similar series of experiments KCl (60 nmol/l) was administered to both control and TRH-'treated' pituitary tissue as a 3-min pulse; no significant differences in TSH responses or prolactin responses were observed. These data indicate that TRH desensitizes the pituitary thyrotroph to a subsequent TRH stimulus but has very little effect on prolactin secretion. J. Endocr. (1984) 101, 101–105

Autoregulation of rat pituitary prolactin secretion demonstrated by a new perfusion method

1982 ◽  
Vol 242 (4) ◽  
pp. E226-E233
Author(s):  
H. A. Zacur ◽  
W. E. Mitch ◽  
J. E. Tyson ◽  
P. T. Ostrow ◽  
G. V. Foster
Keyword(s):  
Prolactin Secretion ◽  
Renal Capsule ◽  
In Vitro Perfusion ◽  
Prolactin Release ◽  
Rat Pituitary ◽  
Inbred Rats ◽  
Pituitary Glands ◽  
Prolactin Content ◽  
Pituitary Prolactin

Regulation of prolactin secretion was investigated by perfusing rat pituitaries in vitro. Two pituitary glands from inbred rats were transplanted beneath the renal capsule of a third recipient rat. Three weeks later, the transplanted kidney was removed and perfused in vitro with a defined cell-free medium. Normal renal function was maintained during perfusion, and cell morphology of the transplants remained unchanged as assessed by electron microscopy. Pituitary prolactin content did not change after 120 min of perfusion despite release of approximately 10 micrograms of hormone. Thyrotropin-releasing hormone (10 ng/ml) did not stimulate prolactin release; dopamine (20 ng/ml) rapidly, but transiently inhibited prolactin release; bromocriptine (20 ng/ml) rapidly and persistently inhibited prolactin release; haloperidol (100 ng/ml) blocked the inhibition by dopamine or bromocriptine, but when given alone inhibited prolactin release. Finally, prolactin release was also inhibited by the presence of 100 and 200 ng/ml, but not 50 ng/ml of NIAMDD RP-1 rat prolactin. It is concluded that in vitro perfusion of transplanted rat pituitaries provides a new model for studying the direct effect of agents on the secretion of prolactin from the pituitary and that rat prolactin and/or its metabolites directly inhibit pituitary prolactin secretion.

In vitro thyrotrophin release with thyrotrophin-releasing hormone and an analogue, DN-1417

1984 ◽  
Vol 106 (1) ◽  
pp. 71-78 ◽  
Author(s):  
Kunio Shiota ◽  
Keiji Yoshida ◽  
Chieko Noguchi ◽  
Ryo Nakayama
Keyword(s):  
Cultured Cells ◽  
Direct Action ◽  
Continuous Exposure ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
High K ◽  
Rat Pituitary ◽  
Pituitary Glands ◽  
The Difference

Abstract. Using dispersed and primarily cultured cells of rat pituitary glands, thyrotrophin (TSH) release by TSH-releasing hormone (TRH) and an analogue, γ - butyrolactone - γ-carbonyl - l - histidyl - l - prolinamide (DN-1417) which is more potent than TRH on central nervous system behavioural paradigms, was examined under conditions of static incubation and superfusion. Static incubations of the cells with different concentrations of DN-1417 (10−7–10−4 m) and TRH (10−10–10−6 m) resulted in a dose-related increase of TSH release and the response to both peptides, in logarithmic doses, was in parallel. The potency of DN-1417 related to TSH release was 0.14–0.26% that of TRH. Maximal TSH release induced by DN-1417 (10−5 m) was slightly but significantly greater than that by TRH (10−7 m) In the presence of 3-isobutyl-1-methylxanthine, the TSH response to either of the peptides was augmented, and the difference in the maximal TSH release by either peptide became insignificant, suggesting that TRH as well as DN-1417 act through the same mechanism of mediation by the cyclic nucleotides. In the superfusion study, a biphasic profile of TSH release was observed during a continuous exposure (100 min) to maximal doses of either the analogue or TRH. The biphasic release of TSH was thought to be specific to TRH action because high K+ produced a different profile of the release. These results indicate that the potency of DN-1417 in TSH release is considerably lower than that of TRH, and also suggest that the direct action of DN-1417 on TSH release is qualitatively similar to that of TRH.

Intraventricular administration of thyrotrophin-releasing hormone (TRH) suppresses prolactin secretion and synthesis: a possible involvement of dopamine release by TRH from rat hypothalamus

1992 ◽  
Vol 133 (1) ◽  
pp. 59-66 ◽  
Author(s):  
H. Ikegami ◽  
H. Jikihara ◽  
K. Koike ◽  
K. Morishige ◽  
H. Kurachi ◽  
...  
Keyword(s):  
Dopamine Release ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Serum Prolactin ◽  
Dependent Manner ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Rat Hypothalamus ◽  
Prolactin Gene ◽  
Gene Transcripts

ABSTRACT The administration of thyrotrophin-releasing hormone (TRH) causes a variety of dopamine-related biological events. To understand the specific role of TRH on rat hypothalamic dopamine neurones, we examined the in-vivo effects of intraventricular (i.c.v.) infusion of TRH on the release and synthesis of prolactin in the rat pituitary gland and on the changes in binding of [3H]MeTRH and dopamine turnover rates in rat hypothalamus. We have also examined the in-vitro effects of TRH on the release of [3H]dopamine from dispersed tuberoinfundibular dopamine neurones. Female rats were treated with i.c.v. infusions of 1 μmol TRH/l daily for 1, 3 and 7 days using Alzet osmotic pumps. Following 7 days of treatment the serum prolactin concentrations were significantly decreased. A reduction in hypothalamic TRH-binding sites (Bmax) was also apparent but the dissociation constant (Kd) was unaffected. Northern blot analysis of total RNA isolated from the pituitary glands of control animals using 32P-labelled prolactin cDNA as a probe indicated the presence of three species of prolactin gene transcripts of approximately 3·7, 2·0 and 1·0 kb in size, and these were decreased by TRH treatment. We examined the turnover rate of dopamine in the rat hypothalamus when TRH was administered i.c.v. for 7 days. There was a significant increase in 3,4-dihydroxyphenylacetic acid/dopamine ratio with TRH treatment. Moreover, exposure to TRH stimulated [3H]dopamine release from rat tuberoinfundibular neurones in a time- and dose-dependent manner. Dopamine receptor antagonists such as SCH23390 and (−)sulpiride, and other neuropeptides such as vasoactive intestinal peptide and oxytocin did not affect TRH-stimulated [3H]dopamine release. These data suggest that i.c.v. administration of TRH might decrease both prolactin secretion and accumulation of prolactin gene transcripts in the pituitary by stimulating dopamine release from tuberoinfundibular neurones. Journal of Endocrinology (1992) 133, 59–66

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