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

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

Stimulatory effect of thyrotrophin-releasing hormone (TRH) on the release of luteinizing hormone (LH) from rat anterior pituitary cells in vitro

1983 ◽  
Vol 61 (2) ◽  
pp. 186-189 ◽  
Author(s):  
Noboru Fujihara ◽  
Masataka Shiino
Keyword(s):  
Luteinizing Hormone ◽  
Anterior Pituitary ◽  
Pituitary Cells ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Anterior Pituitary Cells ◽  
Lh Release ◽  
Lh Rh

The effect of thyrotrophin-releasing hormone (TRH, 10−7 M) on luteinizing hormone (LH) release from rat anterior pituitary cells was examined using organ and primary cell culture. The addition of TRH to the culture medium resulted in a slightly enhanced release of LH from the cultured pituitary tissues. However, the amount of LH release stimulated by TRH was not greater than that produced by luteinizing hormone – releasing hormone (LH–RH, 10−7 M). Actinomycin D (2 × 10−5 M) and cycloheximide (10−4 M) had an inhibitory effect on the action of TRH on LH release. The inability of TRH to elicit gonadotrophin release from the anterior pituitary glands in vivo may partly be due to physiological inhibition of its action by other hypothalamic factor(s).

Effects of synthetic mammalian thyrotrophin releasing hormone, somatostatin and dopamine on the secretion of prolactin and growth hormone from amphibian and reptilian pituitary glands incubated in vitro

1984 ◽  
Vol 102 (2) ◽  
pp. 175-180 ◽  
Author(s):  
T. R. Hall ◽  
A. Chadwick
Keyword(s):  
Rana Catesbeiana ◽  
Apparent Effect ◽  
Lower Vertebrate ◽  
Thyrotrophin Releasing Hormone ◽  
Factors Affecting ◽  
Releasing Hormone ◽  
Hypothalamic Extract ◽  
Pituitary Glands ◽  
Regulation Of Secretion

ABSTRACT Pituitary glands of grassfrog (Rana pipiens), bullfrog (Rana catesbeiana), clawed toad (Xenopus laevis) and two species of terrapin (Chrysemys picta and Pseudemys scripta) were incubated in medium containing hypothalamic extract (HE), thyrotrophin releasing hormone (TRH), somatostatin, dopamine, or combinations of these treatments. Prolactin and GH concentrations in the medium were determined by densitometry after polyacrylamide-gel electrophoretic separation. Hypothalamic extract stimulated secretion of both hormones in all species tested. Thyrotrophin releasing hormone stimulated secretion of prolactin and GH, showing a biphasic pattern of response. Dopamine had little effect alone, but inhibited HE-and TRH-stimulated release of prolactin, but not GH, in both amphibia and reptiles. Somatostatin by itself had no apparent effect on release of hormones, but it inhibited HE- and TRH-stimulated release of GH from both amphibian and reptilian pituitary glands. These results indicate that factors affecting mammals and birds also interact in the regulation of secretion of prolactin and GH in lower vertebrate species. J. Endocr. (1984) 102, 175–180

Effects of two enkephalin analogues, morphine sulphate, dopamine and naloxone on prolactin secretion from rat anterior pituitary glands in vitro

1986 ◽  
Vol 109 (3) ◽  
pp. 313-320 ◽  
Author(s):  
A. M. Bentley ◽  
M. Wallis
Keyword(s):  
Anterior Pituitary ◽  
Time Course ◽  
Opiate Receptors ◽  
Inhibitory Effect ◽  
Antagonistic Effect ◽  
Prolactin Secretion ◽  
Morphine Sulphate ◽  
Low Concentrations ◽  
Pituitary Glands

ABSTRACT Experiments were carried out on the antagonistic effects of opiates on the inhibition by dopamine of prolactin secretion from rat anterior pituitary glands. Dose–response and time-course experiments were carried out using both static incubation of paired hemipituitary glands and perifusion of whole glands. Dopamine (10–1000 nmol/l) was found to have an inhibitory effect on prolactin secretion, but at a lower concentration (0·1 nmol/l) a small stimulation was observed. Against an inhibition established with 100 nmol dopamine/l in static incubation, the three opiates under study, morphine sulphate, Leu5enkephalin and d-Ala2,Met5-enkephalin (DAME), had a maximum antagonistic effect at 50–1000 nmol/l in a 90-min incubation. Morphine and DAME were rather more effective than Leu5-enkephalin, possibly because of degradation of the latter. Naloxone reversed the effect of morphine. All three opiates showed little effect on dopamine-inhibited prolactin secretion in a perifusion system. The data accord with previous suggestions that prolactin secretion may be stimulated both by very low concentrations of dopamine and by opiates acting to reverse the inhibition exerted by higher dopamine concentrations. It should be noted that both morphine and the enkephalins have similar effects on prolactin secretion, despite their normal specificity for different opiate receptors; their actions on the pituitary may thus be rather non-specific. J. Endocr. (1986) 109, 313–320

pGlutamylglutamylprolineamide modulation of growth hormone secretion in domestic fowl: antagonism of thyrotrophin-releasing hormone action?

1993 ◽  
Vol 138 (1) ◽  
pp. 137-147 ◽  
Author(s):  
S. Harvey ◽  
V. L. Trudeau ◽  
R. J. Ashworth ◽  
S. M. Cockle
Keyword(s):  
Domestic Fowl ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Concomitant Administration ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Pituitary Glands ◽  
First Time

ABSTRACT Pyroglutamylglutamylprolineamide (pGlu-Glu-ProNH2) is a tripeptide with structural and immunological similarities to thyrotrophin-releasing hormone (TRH; pGlu-His-ProNH2). Since TRH stimulates GH secretion in domestic fowl, the possibility that pGlu-Glu-ProNH2 may also provoke GH release was investigated. Unlike TRH, pGlu-Glu-ProNH2 alone had no effect on GH release from incubated chicken pituitary glands and did not down-regulate pituitary TRH receptors. However, pGlu-Glu-ProNH2 suppressed TRH-induced GH release from pituitary glands incubated in vitro and competitively displaced [3H]methyl3-histidine2-TRH from pituitary membranes. Systemic injections of pGlu-Glu-ProNH2 had no significant effect on basal GH concentrations in conscious birds, but promptly lowered circulating GH levels in sodiumpentobarbitone anaesthetized fowl. Submaximal GH responses of conscious and anaesthetized birds to systemic TRH challenge were, however, potentiated by prior or concomitant administration of pGlu-Glu-ProNH2. These results demonstrate, for the first time, that pGlu-Glu-ProNH2 has biological activity, with inhibitory and stimulatory actions within the avian hypothalamo-pituitary axis. These results indicate that pGlu-Glu-ProNH2 may act as a TRH receptor antagonist within this axis. Journal of Endocrinology (1993) 138, 137–147

Alteration by thyrotrophin-releasing hormone of heterogeneous components associated with thyrotrophin biosynthesis in the rat anterior pituitary gland

1984 ◽  
Vol 103 (2) ◽  
pp. 165-171 ◽  
Author(s):  
M. Mori ◽  
M. Murakami ◽  
T. Iriuchijima ◽  
H. Ishihara ◽  
I. Kobayashi ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
De Novo ◽  
Close Association ◽  
Anterior Pituitary Gland ◽  
Male Rats ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Pituitary Glands

ABSTRACT An influence of thyrotrophin-releasing hormone (TRH) on TSH heterogeneity in close association with de-novo biosynthesis was studied in rat anterior pituitary glands. Hemipituitary glands from adult male rats were incubated in Krebs–Henseleit–glucose media containing [3H]glucosamine and [14C]alanine for 3 and 6 h in the presence or absence of 10 ng TRH per ml. Fractions of TSH in the pituitary extracts were obtained using affinity chromatography coupled with an anti-rat TSH globulin. These TSH fractions were analysed by isoelectric focusing. The control pituitary glands were composed of four component peaks (isoelectric point (pI) 8·7, 7·8, 5·3 and 2·5) of [3H]glucosamine and [14C]alanine incorporated into TSH, and the amounts of radioactivity of these components were increased with the incubation time. Of these peaks, radioactive components of pI 8·7 and 7·8 coincided with the non-radioactive TSH components measured by radioimmunoassay. Addition of TRH increased incorporation of [14C]alanine into TSH in each of the components to a greater extent than that of [3H]glucosamine. In addition, new components with pI 7·2, 6·5 and 6·2, each component corresponding to each unlabelled TSH component, were demonstrated in the presence of TRH. Because addition of TRH did not change the amounts of [14C]alanine-labelled TSH in the media, the newly formed components were assumed to be connected with protein synthesis occurring in the anterior pituitary gland, which may be specific substances in response to TRH administration. These results indicate that TRH principally elicits an increase in protein synthesis in TSH at the anterior pituitary level, resulting in an alteration of TSH heterogeneity. J. Endocr. (1984) 103, 165–171

INFLUENCE OF ANAESTHETICS ON BASAL, PERPHENAZINE-INDUCED AND THYROTROPHIN RELEASING HORMONE-INDUCED PROLACTIN SECRETION IN OVARIECTOMIZED, OESTROGEN-TREATED RATS

1975 ◽  
Vol 66 (2) ◽  
pp. 151-157 ◽  
Author(s):  
D. M. LAWSON ◽  
R. R. GALA
Keyword(s):  
Central Nervous System ◽  
Anterior Pituitary ◽  
Chloral Hydrate ◽  
Direct Action ◽  
Prolactin Secretion ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Site Of Action ◽  
The Central Nervous System ◽  
Normal Increase

SUMMARY Plasma levels of prolactin were determined, by radioimmunoassay, in ovariectomized, oestrogen-treated rats after administration of ether, sodium pentobarbitone, urethane, chloral hydrate or ketamine. These anaesthetics, when administered alone, induced sustained increases in the plasma level of prolactin (continuous ether inhalation), no change in prolactin secretion (urethane), or depressions in the level of prolactin (sodium pentobarbitone, chloral hydrate and ketamine). These same anaesthetics when given before perphenazine failed to alter the stimulatory effect of this phenothiazine on prolactin secretion. Sodium pentobarbitone did not alter the normal increase in prolactin concentration after intra-arterial administration of synthetic thyrotrophin releasing hormone (TRH). These results indicated that anaesthetics do not affect the response of either the central nervous system or the anterior pituitary to perphenazine or TRH although they affect prolactin secretion when administered alone. The site of action of anaesthetics must, therefore, be different from that of perphenazine or perphenazine must be capable of overcoming their influence by direct action on the pituitary.

The effect of neurotensin on pituitary secretion of thyrotrophin and prolactin in vitro

1984 ◽  
Vol 105 (2) ◽  
pp. 156-160 ◽  
Author(s):  
R. D. Askew ◽  
D. B. Ramsden ◽  
M. C. Sheppard
Keyword(s):  
Anterior Pituitary ◽  
Inhibitory Effect ◽  
Pituitary Cells ◽  
Basal Secretion ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Direct Inhibitory Effect ◽  
In Vitro Systems ◽  
Pituitary Secretion

Abstract. The effects of neurotensin on thyrotrophin (TSH) and prolactin (Prl) release were studied in two in vitro systems – anterior pituitary cells in culture and perifused anterior pituitary fragments. Neurotensin significantly reduced basal secretion of both TSH and Prl (P < 0.001) from cultured pituitary cells, and abolished thyrotrophin releasing hormone (TRH)-stimulated TSH release. Neurotensin significantly reduced TRH-stimulated TSH and Prl release (P < 0.02) from perifused pituitary fragments. These data indicate that neurotensin has a direct inhibitory effect on TSH and Prl secretion by the anterior pituitary.

INHIBITION BY CORTISOL OF ACTH RELEASE FROM ANTERIOR PITUITARY TISSUE IN VITRO

1966 ◽  
Vol 44 (4) ◽  
pp. 549-556 ◽  
Author(s):  
John J. Pollock ◽  
Frank S. LaBella
Keyword(s):  
Adrenal Cortex ◽  
Incubation Medium ◽  
Anterior Pituitary ◽  
Pituitary Tissue ◽  
Pituitary Glands ◽  
Cortex Slices ◽  
Acth Release

The central basophilic region of bovine anterior pituitary glands was incubated for 30 minutes with varying concentrations of cortisol. Dialyzed incubation medium was subsequently assayed for ACTH activity by measuring the increased production of steroids from bovine adrenal cortex slices. Inhibition of ACTH release was evident with 5.5 × 10−11 M cortisol, but was more pronounced and consistent with 5.5 × 10−8 M or higher. Concentrations of 5.5 × 10−6 and 5.5 × 10−5 M were generally less effective in causing inhibition of ACTH release than were concentrations of 5.5 × 10−8 and 5.5 × 10−7 M.

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