Hypothalamic dopamine and catechol oestrogens in rats with spontaneous pituitary tumours

1983 ◽  
Vol 96 (2) ◽  
pp. 347-352 ◽  
Author(s):  
R. A. Prysor-Jones ◽  
J. J. Silverlight ◽  
J. S. Jenkins
Keyword(s):  
Pituitary Gland ◽  
Plasma Prolactin ◽  
Pituitary Tumours ◽  
Dopamine Concentration ◽  
Rat Pituitary ◽  
Pituitary Glands ◽  
Normal Rat ◽  
Old Rats ◽  
Hypothalamic Dopamine

Dopamine concentration within the hypothalamus and its depletion after the administration of α-methyl-para-tyrosine were measured in young rats and compared with values obtained in aged animals with and without spontaneously occurring pituitary tumours. Old rats had significantly reduced hypothalamic dopamine concentrations and there was less depletion of dopamine compared with young animals but there were no differences between tumorous and non-tumorous animals. Hyperprolactinaemia induced in young animals caused a much greater depletion of hypothalamic dopamine than in old tumorous rats with comparable plasma prolactin concentrations. The catechol oestrogen 2-hydroxyoestradiol inhibited the release of prolactin from normal rat pituitary glands in vitro but measurement of catechol oestrogens in the hypothalamus showed no differences between young and old tumorous or non-tumorous rats. It is concluded that reduced dopamine concentration and an impaired response to hyperprolactinaemia in old rats may facilitate the growth of prolactin-secreting tumours arising in the pituitary gland.

Effect of tamoxifen on growth and prolactin secretion of rat pituitary tumours

1983 ◽  
Vol 97 (2) ◽  
pp. 261-266 ◽  
Author(s):  
R. A. Prysor-Jones ◽  
J. J. Silverlight ◽  
J. S. Jenkins
Keyword(s):  
Dna Synthesis ◽  
Dopamine Agonist ◽  
Pituitary Adenomas ◽  
Tumour Growth ◽  
Prolactin Secretion ◽  
Moderate Increase ◽  
Plasma Prolactin ◽  
Pituitary Tumours ◽  
Rat Pituitary

The antioestrogenic drug tamoxifen was administered to rats bearing transplanted prolactin-secreting tumours derived from spontaneously occurring pituitary adenomas in Wistar–Furth rats. Some inhibition of tumour growth was observed but this was accompanied by an increase in plasma prolactin concentrations. Bromocriptine, however, consistently inhibited both growth and prolactin secretion of these tumours. The addition of tamoxifen to bromocriptine treatment produced no increased response to the dopamine agonist. Tamoxifen increased prolactin secretion by tumour cells in vitro but did not affect DNA synthesis. Normal rats responded to tamoxifen with a moderate increase in plasma prolactin concentrations and there was no change in pituitary DNA synthesis.

The involvement of ovarian factors in maintaining the pituitary glands of female rats in a state of low LH responsiveness to LHRH

1987 ◽  
Vol 112 (2) ◽  
pp. 265-273 ◽  
Author(s):  
J. de Koning ◽  
A. M. I. Tijssen ◽  
G. P. van Rees
Keyword(s):  
Pituitary Gland ◽  
Phase Response ◽  
The Self ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Lag Phase ◽  
Second Phase ◽  
Rat Pituitary ◽  
Pituitary Glands

ABSTRACT The effects of discontinuation and restoration of ovarian influences on the pituitary LH response to LHRH in vitro were investigated. When female rat pituitary glands taken on day 2 of dioestrus were incubated with LHRH the release of LH was low during the first hour (lag phase response) and afterwards a progressive, protein synthesis-dependent increase took place (second phase response), this being the self-priming action of LHRH. Short-term discontinuation (less than 1 day) of ovarian influences on the rat pituitary gland in vivo (ovariectomy) or in vitro (incubation in medium only) resulted in an increased LHRH-induced LH response during the lag phase. The biphasic LH response or the self-priming action of LHRH disappeared completely after long-term discontinuation of ovarian influences on the pituitary gland, LH release being at its maximum from the start of the incubation. The biphasic response was reinstated when ovaries were implanted under the kidney capsules of ovariectomized rats. Auto-implantation of an ovary into the spleen immediately after bilateral ovariectomy did not, however, prevent the disappearance of the LHRH self-priming action. Ovarian activity responsible for the presence of the low LH response during the lag phase was thus effectively removed by the liver, but inhibin-like activity suppressing serum FSH levels remained present. Silicone elastomer implants (s.c.) containing oestradiol-17β, implanted for 4 weeks, did not reverse the loss of the biphasic LH response to LHRH. It is concluded that liver-labile factors released by the ovaries keep the pituitary gland in a state of low responsiveness to LHRH. By giving a sufficiently high LHRH stimulus this inhibitory effect is neutralized and transition to a highly responsive state can be achieved. The ovarian factor(s) is not identical to inhibin or oestradiol-17β. J. Endocr. (1987) 112, 265–273

EFFECT OF 6-DEHYDRO-16-METHYLENE-HYDROCORTISONE AND DEXAMETHASONE ON THE RELEASE OF ACTH FROM RAT PITUITARY GLANDS IN VITRO

1970 ◽  
Vol 63 (3) ◽  
pp. 431-436 ◽  
Author(s):  
K. Berthold ◽  
A. Arimura ◽  
A. V. Schally
Keyword(s):  
Pituitary Gland ◽  
Direct Action ◽  
Rat Pituitary ◽  
Pituitary Glands ◽  
Acth Release

ABSTRACT Direct action of 6-dehydro-16-methylene-hydrocortisone (STC 407) and dexamethasone on the rat pituitary gland was investigated in vitro. CRF-induced ACTH release was suppressed after preincubation of the pituitary gland with 10 μg STC 407/ml or 1 μg dexamethasone/ml. These results suggest that both STC 407 and dexamethasone act directly on the pituitary gland.

DIFFERENCES IN THE RELEASE OF MELANOCYTE-STIMULATING HORMONE IN VITRO BY RAT PITUITARY GLANDS COLLECTED AT VARIOUS TIMES DURING THE OESTROUS CYCLE

1978 ◽  
Vol 78 (1) ◽  
pp. 1-6 ◽  
Author(s):  
ADRIANA VIVAS ◽  
MARÍA ESTER CELIS
Keyword(s):  
Pituitary Gland ◽  
Oestrous Cycle ◽  
Biological Assay ◽  
Melanocyte Stimulating Hormone ◽  
Pituitary Tissue ◽  
Rat Pituitary ◽  
Pituitary Glands ◽  
Stimulating Hormone

The release of melanocyte-stimulating hormone (MSH) into the medium during incubation and the pituitary tissue content of MSH were measured separately using pituitary glands collected from rats at various stages of the oestrous cycle. The MSH was measured by a biological assay using a synthetic α-MSH as standard. The release of MSH was maximal during the pro-oestrous phase and MSH content of the pituitary gland was highest during dioestrus. The influences of the tripeptide Pro-Leu-Gly-NH2, which inhibits MSH secretion in vivo, and of progesterone on the release of MSH in vitro were studied with tissue collected at various phases of the oestrous cycle. Pro-Leu-Gly-NH2 was effective in inhibiting MSH release both at pro-oestrus and oestrus but not at dioestrus. Progesterone overcame this inhibition.

In-vivo and in-vitro secretion of prolactin by lactating rat adenohypophyses as a function of intracellular age

1984 ◽  
Vol 101 (1) ◽  
pp. 27-32 ◽  
Author(s):  
F. Mena ◽  
G. Martínez-Escalera ◽  
C. Clapp ◽  
C. E. Grosvenor
Keyword(s):  
Pituitary Gland ◽  
Incubation Period ◽  
Gel Electrophoresis ◽  
Polyacrylamide Gel Electrophoresis ◽  
Polyacrylamide Gel ◽  
Pituitary Glands ◽  
H 26

ABSTRACT Adenohypophysial prolactin of lactating rats was pulse-labelled by [3H]leucine injected i.v. at the time of removal of the pups. The [3H]prolactin concentration in the pituitary gland, analysed by polyacrylamide-gel electrophoresis, progressively fell as the time from labelling to removal of the pituitary gland increased from 8 to 24 h, which suggests that there was a loss of hormone as it aged within the gland. Suckling effectively provoked the depletion–transformation of total and [3H]prolactin (extracted at pH 7·2) when applied after 8 h but not when applied after either 16 or 24 h after removing the pups. In rats whose pups were removed for 8 h, suckling also depleted–transformed [3H]prolactin labelled 4 h, but not that labelled 1 h before suckling. The pituitary glands of other lactating rats were labelled with [3H]leucine injected i.v. at various times before removing the glands and incubating them in medium 199. The secretion into the medium of [3H]prolactin labelled either 4, 8, 16 or 24 h beforehand was maximal during the first 30 min then declined from 30 to 240 min of incubation. However, secretion of prolactin labelled 1 h and 10 min beforehand reached a maximum after 0·5–1 h and 2 h of incubation respectively, then remained constant during the remainder of the 4-h incubation period. The total 4-h secretion of [3H]prolactin was greatest (65% of preincubation concentration) from those glands labelled 4 h before in contrast to those labelled 10 min (15%) or 1 (38%), 8 (34%), 16 (18%) or 24 h (26%) before incubation. Taken together, these data suggest that prolactin synthesized 4 h earlier is more likely to be released in response to physiological stimuli than is more recently formed prolactin or prolactin which has remained in the pituitary gland for 16 h or longer. J. Endocr. (1984) 101, 27–32

scholarly journals Tyrosine Hydroxylase and Dopamine Transporter Expression in Lactotrophs from Postlactating Rats: Involvement in Dopamine-Induced Apoptosis

Endocrinology ◽  
2007 ◽  
Vol 148 (6) ◽  
pp. 2698-2707 ◽  
Author(s):  
Arnaud Jaubert ◽  
Guillaume Drutel ◽  
Thierry Leste-Lasserre ◽  
François Ichas ◽  
Laurence Bresson-Bepoldin
Keyword(s):  
Tyrosine Hydroxylase ◽  
Pituitary Gland ◽  
Caspase 3 ◽  
D2 Receptor ◽  
Prolactin Secretion ◽  
Rat Pituitary ◽  
Pituitary Glands ◽  
Mitochondrial Membrane Potential Loss ◽  
Induced Apoptosis ◽  
Transporter Expression

Cessation of lactation causes a massive loss of surplus lactotrophs in the rat pituitary gland. The factors and mechanisms involved in this phenomenon have not yet been elucidated. Besides its inhibitory control on prolactin secretion and lactotroph proliferation, evidence suggests that dopamine (DA) may be a proapoptotic factor for lactotrophs. We therefore tested the proapoptotic effect of DA on pituitary glands from virgin, lactating, and postlactating rats. By measuring mitochondrial membrane potential loss, caspase-3 activation, and nuclear fragmentation, we show that DA induces apoptosis specifically in lactotrophs from postlactating rats. We then determined that this effect was partly mediated by the DA transporter (DAT) rather than the D2 receptor, as corroborated by the detection of DAT expression exclusively in lactotrophs from postlactating rats. We also observed tyrosine hydroxylase (TH) expression in postlactating lactotrophs that was accompanied by an increase in DA content in the anterior pituitary gland of postlactating compared with virgin rats. Finally, we observed that cells expressing TH coexpressed DAT and cleaved caspase-3. These findings show that DA may play a role in lactotroph regression during the postlactation period by inducing apoptosis. The fact that this process requires DAT and TH expression by lactotrophs themselves suggests that it may be “autocrine” in nature.

Homologous and heterologous regulation of somatostatin-binding sites on chicken adenohypophysial membranes

1990 ◽  
Vol 127 (3) ◽  
pp. 417-425 ◽  
Author(s):  
S. Harvey ◽  
J. S. Baidwan ◽  
D. Attardo
Keyword(s):  
Pituitary Gland ◽  
Binding Sites ◽  
Recombinant Dna ◽  
Inhibitory Effect ◽  
Partial Recovery ◽  
Caudal Lobe ◽  
Direct Inhibitory Effect ◽  
Pituitary Glands

ABSTRACT Binding of 125I-labelled [Tyr1]-somatostatin (125I-[Tyr1]-SRIF) to pituitary caudal lobe membranes was suppressed in immature chickens 1 and 2 h after i.v. administration of unlabelled SRIF at concentrations of 1–100 μg/kg. In-vitro preincubation of chicken pituitary glands for 0·5–4·0 h with 0·1 μmol SRIF/l similarly reduced the binding of 125I-[Tyr1]-SRIF to caudal lobe membrane preparations. After a 4-h incubation in 0·1 mmol SRIF/l, the withdrawal of SRIF from the incubation media was accompanied 4 h later by a partial recovery in the binding of 125I-[Tyr1]-SRIF to pituitary membranes. Passive immunoneutralization of endogenous SRIF resulted in a prompt (within 1 h) and sustained (for at least 24 h) suppression of 125I-[Tyr1]-SRIF binding to pituitary membranes. The i.m. administration of cysteamine (300 mg/kg) to 12-week-old birds depleted hypothalamic SRIF stores and decreased the density of 125I-[Tyr1]-SRIF-binding sites in the caudal and cephalic lobes of the chicken pituitary gland. The reduction in SRIF content and in SRIF-binding sites occurred within 1 h of cysteamine administration and was maintained for at least 24 h. In 6-week-old birds, cysteamine (300 mg/kg) administration suppressed pituitary binding of 125I-[Tyr1]-SRIF for at least 5 days. Circulati concentrations of GH were markedly decreased 1 and 4 h after cysteamine injection, but not after 24 h. Pituitary binding sites for 125I-[Tyr1]-SRIF were not affected by pretreatment of pituitary glands for 2–12 h in vitro with thyroxine or oestradiol-17β (1 nmol/l–10 μmol/l) or with ovine GH or recombinant DNA-derived chicken GH (1–100 μg/ml in vitro and 100–1000 μg/kg in vivo). Ovine prolactin, at concentrations of 1–100 μg/ml was also without effect on 125I-[Tyr1]-SRIF binding to pituitary membranes following a 2- or 4-h incubation with pituitary glands. Pituitary binding sites for 125I-[Tyr1]-SRIF were, however, increased after a 24-h incubation with 1 μmol tri-iodothyronine (T3)/l in vitro and 4 and 24 h after the administration of T3 (100–1000 μg/kg) in vivo. Although T3 had no direct inhibitory effect on 125I-[Tyr1]-SRIF binding to pituitary membranes, binding was suppressed 1 and 2 h after the in-vivo administration of T3 at concentrations of 100–1000 μg/kg. These results therefore demonstrate homologous and heterologous regulation of SRIF-binding sites in the chicken pituitary gland. Journal of Endocrinology (1990) 127, 417–425

2-HYDROXYOESTRADIOL INHIBITS PROLACTIN RELEASE FROM THE SUPERFUSED RAT PITUITARY GLAND

1981 ◽  
Vol 90 (3) ◽  
pp. 315-322 ◽  
Author(s):  
ELIZABETH A. LINTON ◽  
NICKI WHITE ◽  
OFELIA LIRA DE TINEO ◽  
S. L. JEFFCOATE
Keyword(s):  
Pituitary Gland ◽  
Prolactin Secretion ◽  
Male Rat ◽  
Prolactin Release ◽  
Rat Pituitary ◽  
Lh Release

The effects of 2-hydroxyoestradiol (2OH-OE2), dopamine, oestradiol-17β and 2OH-OE2 plus dopamine on prolactin and LH release from the male rat pituitary gland were examined in vitro. 2-Hydroxyoestradiol reduced prolactin secretion by 51% at 10−10 mol/l and by 34% at 10−7 mol/l, while oestradiol-17β had no effect at these doses. Dopamine alone (5 × 10−7 mol/l) decreased prolactin released by 58%, 2OH-OE2 plus dopamine produced a similar inhibition of 60%. No significant effect on LH release was observed throughout.

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