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.

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

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

DEMONSTRATION OF THYROTROPHIN β-SUBUNIT MESSENGER RNA IN RAT PITUITARY CELLS IN PRIMARY CULTURE - EVIDENCE FOR REGULATION BY THYROTROPHIN-RELEASING HORMONE AND FORSKOLIN

1986 ◽  
Vol 111 (1) ◽  
pp. R1-R2 ◽  
Author(s):  
J.A. Franklyn ◽  
M. Wilson ◽  
J.R. Davis ◽  
D.B. Ramsden ◽  
K. Docherty ◽  
...  
Keyword(s):  
Primary Culture ◽  
Messenger Rna ◽  
Pituitary Cells ◽  
Adenylate Cyclase System ◽  
Β Subunit ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

ABSTRACT We have reported previously the effect of thyroid status in vivo on pituitary cytoplasmic concentrations of messenger RNA (mRNA) encoding the thyrotrophin (TSH) β-subunit (Franklyn, Lynam, Docherty et al, 1985). Studies in vitro of the regulation of TSH β gene transcription have been confined to thyrotrophic tumour cells. We now report the demonstration of TSH β-subunit mRNA in non-tumorous rat pituitary cells in primary culture. Treatment of cells with thyrotrophin-releasing hormone (TRH) and with forskolin resulted in a marked increase in cellular concentration of TSH β-mRNA. These results suggest that TRH exerts a direct effect on the pretranslational events involved in TSH synthesis and further that the adenylate cyclase system may be involved in the regulation of synthesis. We have thus described a novel system for the study of TSH β-subunit gene expression in normal rat pituitary cells in vitro.

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.

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

Mechanisms of release of prolactin from fowl anterior pituitary glands incubated in vitro: effects of calcium and cyclic adenosine monophosphate

1985 ◽  
Vol 105 (2) ◽  
pp. 183-188 ◽  
Author(s):  
T. R. Hall ◽  
S. Harvey ◽  
A. Chadwick
Keyword(s):  
Cyclic Amp ◽  
Anterior Pituitary ◽  
Phosphodiesterase Inhibitor ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Thyrotrophin Releasing Hormone ◽  
Hypothalamic Extract ◽  
High K ◽  
Pituitary Glands

ABSTRACT Fowl anterior pituitary glands were bisected and each half was pretreated in either Medium 199 or medium containing EGTA to deplete endogenous calcium (Ca2+) stores, after which they were incubated in Medium 199, or Ca2+-free medium, containing prolactin release-stimulating agents and verapamil, a Ca2+ channel blocker. High K+ concentrations, hypothalamic extract, synthetic thyrotrophin-releasing hormone (TRH) and dibutyryl cyclic AMP (dbcAMP) all stimulated release of prolactin from control (non EGTA-treated) hemianterior pituitary glands. The effects of TRH and dbcAMP were not additive, but the response to submaximal concentrations of TRH was augmented by theophylline, a phosphodiesterase inhibitor. Reduction of Ca2+ availability with EGTA or verapamil reduced basal release of prolactin, prevented the prolactin-stimulating effects of high K+ concentrations and TRH, and markedly attenuated responses to hypothalamic extract and dbcAMP, EGTA being more effective than verapamil. Increasing the Ca2+ concentration of the medium did not augment basal or stimulated release of prolactin. These results suggest that both Ca2+ and cyclic AMP may act as intracellular mediators in the release of prolactin. Both basal and stimulated release of prolactin depend upon the presence of Ca2+. Although influx from the medium may be the major source of Ca2+, endogenous stores of Ca2+, perhaps mobilized by dbcAMP, may be able to maintain some release of prolactin. The prolactin-stimulating effects of TRH may be mediated by cyclic AMP. J. Endocr. (1985) 105, 183–188

IMMATURE RAT PITUITARY GLANDS IN VITRO: AGE- AND SEX-RELATED CHANGES IN LUTEINIZING HORMONE RELEASING HORMONE-STIMULATED GONADOTROPHIN RELEASE

1977 ◽  
Vol 73 (2) ◽  
pp. 309-319 ◽  
Author(s):  
J. DULLAART
Keyword(s):  
Male Rats ◽  
Steady Increase ◽  
Releasing Hormone ◽  
Rat Pituitary ◽  
Pituitary Glands ◽  
Lh Release ◽  
The One ◽  
Lh Rh ◽  
Lh Releasing Hormone

SUMMARY Pituitary glands from immature female and male rats aged between 5 and 30 days were incubated in vitro and the effect of LH releasing hormone (RH) on the release of LH and FSH was studied. Pituitary gonadotrophin contents were also measured. Gonadotrophin release showed changes with age as well as sex differences: after LH-RH stimulation the female pattern of release of LH and FSH (expressed per mg pituitary tissue) showed a peak at day 15; the male pattern of LH release was characterized by a steady increase with age, whereas FSH release stayed more or less constant from day 10 onwards. In both sexes the LH:FSH ratio increased with age, both in pituitary gonadotrophin content and in the mixture of gonadotrophins released. It is discussed, that the prepubertal development of pituitary gonadotrophic function might be determined on the one hand by rather autonomous growth processes (more or less similar in female and male hypophyses) and on the other hand by modulating influences of sex steroid hormones, which are different in female and male animals.

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

DIFFERENT EFFECTS OF ORAL DOSES OF TRIIODOTHYRONINE OR THYROXINE ON THE INHIBITION OF THYROTROPHIN RELEASING HORMONE (TRH) MEDIATED THYROTROPHIN (TSH) RESPONSE IN MAN

1975 ◽  
Vol 80 (1) ◽  
pp. 42-48 ◽  
Author(s):  
K. W. Wenzel ◽  
H. Meinhold ◽  
H. Schleusener
Keyword(s):  
Oral Administration ◽  
Binding Sites ◽  
Direct Action ◽  
Normal Range ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Pituitary Tissue ◽  
Tsh Secretion ◽  
Inhibiting Protein ◽  
Oral Doses

ABSTRACT Since contradicting results about the existence of T3 or T3 and T4 receptors in pituitary tissue have been reported, the influence of L-triiodothyronine (L-T3) or L-thyroxine (L-T4) on TRH stimulated TSH release was investigated. Oral administration of 50 μg L-T3 caused an increasing inhibition of TSH response to 400 μg TRH from 64 % 2 h after L-T3 intake to 29% after 24 h, while serum T3 peaks up to 5.45 ng/ml occurred between 2 to 4 h after L-T3 ingestion and became normal after 8 to 10 h. This delay in the T3 action on TRH inhibition agrees with the postulate that T3 induces the synthesis of an inhibiting protein which is blocking TSH liberation. Oral administration of 1000 μg L-T4 induced increments of serum T4 up to 221 ng/ml between 6 to 24 h after intake; however, a TRH inhibition of 62 % did not become evident before 48 h. At this time T3 levels had risen to the upper normal range. These results support the theory that T3 is responsible for the regulation of TSH secretion. An intra-pituitary conversion from T4 to T3 seems more likely the cause of the TRH inhibition rather than the peripheral T4-T3 conversion or a direct action by T4 binding sites in the pituitary.

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