scholarly journals INHIBITION BY PENTOBARBITONE AND URETHANE OF THE in vitro RESPONSE OF THE ADENOHYPOPHYSIS TO LUTEINISING HORMONE-RELEASING HORMONE IN MALE RATS

1979 ◽  
Vol 67 (2) ◽  
pp. 277-281 ◽  
Author(s):  
D.A. CARTER ◽  
R.G. DYER
Keyword(s):  
Luteinising Hormone ◽  
Male Rats ◽  
Releasing Hormone ◽  
In Vitro Response

Sensitisation of pituitary cells to luteinising hormone releasing hormone by clomiphene citrate in vitro

Nature ◽  
1978 ◽  
Vol 273 (5657) ◽  
pp. 57-59 ◽  
Author(s):  
A. J. W. HSUEH ◽  
G. F. ERICKSON ◽  
S. S. C. YEN
Keyword(s):  
Luteinising Hormone ◽  
Clomiphene Citrate ◽  
Pituitary Cells ◽  
Releasing Hormone

THE EFFECTS OF TESTOSTERONE AND ITS 5α-REDUCED METABOLITES ON PITUITARY RESPONSIVENESS TO GONADOTROPHIN-RELEASING HORMONE (Gn-RH)

1977 ◽  
Vol 86 (4) ◽  
pp. 728-732 ◽  
Author(s):  
Y. Epstein ◽  
B. Lunenfeld ◽  
Z. Kraiem
Keyword(s):  
Pituitary Gland ◽  
Mature Male ◽  
Male Rats ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone ◽  
Low Levels ◽  
High Doses ◽  
Dose Dependent ◽  
Stimulation Of

ABSTRACT The aim of this study was to investigate effects of androgens on gonadotrophin release in response to gonadotrophin-releasing hormone (Gn-RH) stimulation in vitro. Hemipituitaries of mature male rats were pre-incubated for 90 min with T, DHT, 3α- or 3β-diol (4 ng or 4 μg/ml medium), and the incubation continued for 240 min after adding Gn-RH (1 ng/ml medium). Gn-RH caused a 4-5-fold rise in the secretion of LH and a 2-fold rise in FSH secretion. The effect of the androgens was dose-dependent. At low levels, T and DHT exerted no effect on Gn-RH-stimulated gonadotrophin release, whereas the two androstanediols (3α- and 3β-diol) augmented the Gn-RH stimulation of both gonadotrophins, though preferentially LH. With high doses of androgens, the results obtained showed: a) no effect of T; b) DHT suppression of the Gn-RH-stimulated FSH release; c) suppression of Gn-RH stimulation by 3α- and 3β-diol regarding both LH and FSH. It is concluded that T exerts through its reduced metabolites a feedback effect on the pituitary gland responsiveness to Gn-RH stimulation.

EFFECT OF VARIOUS PUTATIVE NEUROTRANSMITTERS ON THE SECRETION OF CORTICOTROPHIN-RELEASING HORMONE FROM THE RAT HYPOTHALAMUS IN VITRO – A MODEL OF THE NEUROTRANSMITTERS INVOLVED

1976 ◽  
Vol 69 (1) ◽  
pp. 1-10 ◽  
Author(s):  
M. T. JONES ◽  
E. W. HILLHOUSE ◽  
JANET BURDEN
Keyword(s):  
Median Eminence ◽  
Incubation Medium ◽  
Direct Action ◽  
Aminobutyric Acid ◽  
Male Rats ◽  
Releasing Hormone ◽  
Inhibitory Neurotransmitters ◽  
Basal Release ◽  
Dose Dependent

SUMMARY The effect of incubating the hypothalamus of adult male rats with various neurotransmitters upon the release of corticotrophin-releasing hormone (CRH) was studied. The CRH activity in the incubation medium was assayed in 48 h median eminence-lesioned rats and the corticosteroidogenesis of excised adrenals in vitro was used as the end-point. 5-Hydroxytryptamine (100 pg/ml–10 ng/ml) caused a dose-dependent release of CRH which was antagonized by methysergide (30–100 ng/ml). The response to 5-hydroxytryptamine was also inhibited by hexamethonium and atropine which indicated that it was acting through a cholinergic interneurone. Melatonin (10 ng) did not alter the basal release of CRH but inhibited the action of both 5-hydroxytryptamine (10 ng) and acetylcholine (3 pg). Thus it appears that both 5-hydroxytryptamine and melatonin play a role in the control of CRH release. Noradrenaline blocked the release of CRH induced by both acetylcholine and 5-hydroxytryptamine and presumably this inhibition was caused by direct action on the CRH neurone. γ-Aminobutyric acid (GABA) also inhibited the release of CRH and may also be involved in the regulation of CRH secretion. The inhibitory neurotransmitters, noradrenaline, GABA and melatonin, act via independent receptor mechanisms. A model based on the above data is presented.

Serotonin induces gonadotrophin release through stimulation of LH-releasing hormone release from the median eminence

1986 ◽  
Vol 111 (2) ◽  
pp. 309-315 ◽  
Author(s):  
M. L. Vitale ◽  
M. N. Parisi ◽  
S. R. Chiocchio ◽  
J. H. Tramezzani
Keyword(s):  
Median Eminence ◽  
Anterior Pituitary ◽  
Female Rats ◽  
Male Rats ◽  
Tissue Samples ◽  
Releasing Hormone ◽  
The Third ◽  
Lh Releasing Hormone ◽  
Perifusion System

ABSTRACT The effects of serotonin (5-HT) on the release of gonadotrophins and LH-releasing hormone (LHRH) were examined in an in-vitro perifusion system using median eminences and/or anterior pituitaries obtained from male or pro-oestrous female rats. Animals were killed by decapitation between 12.00 and 13.00 h. A serial double-chamber perifusion system was employed. Three types of experiments were performed. In the first, median eminences were placed in the first chamber and one anterior pituitary in the second chamber. In the second group, only the anterior pituitary was perifused. In the third group, only five median eminences were perifused. In the first and second experiments, LH, FSH and prolactin were determined in the perifusion efflux by radioimmunoassay (RIA). In the third experiment, LHRH was determined by RIA. Addition of 5-HT (final concentrations 0·06, 0·6 and 6·0μmol/l) into the first chamber containing the median eminences stimulated the release of LH and FSH from the pituitary, but did not affect the levels of prolactin in the effluent in the same experiment (prooestrous rats). The stimulatory effect of 5-HT was blocked by the addition of cyproheptadine (1 μmol/l) in the perifusion fluid. The introduction of 5-HT (0·6 μmol/l) into the tube connecting the first and second chambers did not modify the release of LH, nor did 5-HT added to the pituitaries perifused alone. Injection of 5-HT into the first chamber (median eminences), containing tissue samples from male rats, stimulated LH release, but to a significantly (P< 0·001) lower degree than that found when samples from pro-oestrous females were used (P< 0·0001). When median eminences from pro-oestrous rats were perifused alone, injection of 5-HT produced an immediate release of LHRH which peaked during the first 10 min of collection and lasted for 30 min; in these experiments, a clear relationship existed between dose of 5-HT and release of LHRH (P<0·02). The stimulatory effect of 5-HT was blocked by the addition of cyproheptadine (5 μmol/l) or methiothepin (5 μmol/l). These results demonstrate that 5-HT stimulates gonadotrophin release by acting directly on LHRH terminals in the median eminence from pro-oestrous rats. Furthermore, the effect of 5-HT on LHRH release was dose dependent and was nullified by 5-HT receptor blockers (cyproheptadine and methiothepin). J. Endocr. (1986) 111, 309–315

scholarly journals Fasting and Glucose Effects on Pituitary Leptin Expression

2007 ◽  
Vol 55 (10) ◽  
pp. 1059-1073 ◽  
Author(s):  
Christopher Crane ◽  
Noor Akhter ◽  
Brandy W. Johnson ◽  
Mary Iruthayanathan ◽  
Farhan Syed ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Serum Glucose ◽  
Thyroid Stimulating Hormone ◽  
Male Rats ◽  
Target Cells ◽  
Pituitary Cells ◽  
Releasing Hormone ◽  
Leptin Expression ◽  
Fasted Rats

Leptin, a potent anorexigenic hormone, is found in the anterior pituitary (AP). The aim of this study was to determine whether and how pituitary leptin–bearing cells are regulated by nutritional status. Male rats showed 64% reductions in pituitary leptin mRNA 24 hr after fasting, accompanied by significant (30–50%) reductions in growth hormone (GH), prolactin, and luteinizing hormone (LH), and 70–80% reductions in target cells for gonadotropin-releasing hormone or growth hormone-releasing hormone. There was a 2-fold increase in corticotropes. Subsets (22%) of pituitary cells coexpressed leptin and GH, and <5% coexpressed leptin and LH, prolactin, thyroid-stimulating hormone, or adrenocortico-tropic hormone. Fasting resulted in significant (55–75%) losses in cells with leptin proteins or mRNA, and GH or LH. To determine whether restoration of serum glucose could rescue leptin, LH, and GH, additional fasted rats were given 10% glucose water for 24 hr. Restoring serum glucose in fasted rats resulted in pituitary cell populations with normal levels of leptin and GH and LH cells. Similarly, LH and GH cells were restored in vitro after populations from fasted rats were treated for as little as 1 hr in 10–100 pg/ml leptin. These correlative changes in pituitary leptin, LH, and GH, coupled with leptin's rapid restoration of GH and LH in vitro, suggest that pituitary leptin may signal nutritional changes. Collectively, the findings suggest that pituitary leptin expression could be coupled to glucose sensors like glucokinase to facilitate rapid responses by the neuroendocrine system to nutritional cues. (J Histochem Cytochem 55: 1059–1073, 2007)

Testosterone regulates the secretion of thyrotrophin-releasing hormone (TRH) and TRH precursor in the rat hypothalamic-pituitary axis

1990 ◽  
Vol 125 (2) ◽  
pp. 263-270 ◽  
Author(s):  
A. E. Pekary ◽  
M. Knoble ◽  
N. H. Garcia ◽  
S. Bhasin ◽  
J. M. Hershman
Keyword(s):  
In Vitro Release ◽  
Serum Levels ◽  
Male Rats ◽  
Testosterone Replacement ◽  
Male Rat ◽  
Posterior Pituitary ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Vitro Release

ABSTRACT Orchidectomy has been reported to decrease concentrations of thyrotrophin (TSH) in the circulation of male rats without affecting serum levels of thyroid hormones. To understand the mechanism underlying this observation, we have measured the effect of gonadal status on the in-vitro release of TSH-releasing hormone (TRH) by male rat hypothalamic fragments. Because hormone release rates can be affected by changes in the post-translational processing of the hormonal precursors, we have also studied the corresponding changes in the concentrations of TRH and TRH-Gly, a TRH precursor peptide in hypothalamus and pituitary, by radioimmunoassay. We observed a significant decline in the in-vitro release of TRH from incubated hypothalami 1 week after castration, which was quantitatively reversed by testosterone replacement. Concentrations of TRH and TRH-Gly in the posterior pituitary, on the other hand, which derive from neurones of hypothalamic origin, increased significantly with castration and were returned to the normal range by testosterone replacement. We conclude that the primary effect of testosterone is the stimulation of hypothalamic TRH release, resulting in the depletion of TRH and TRH precursors from TRH-containing neurones which project into the median eminence and posterior pituitary. Journal of Endocrinology (1990) 125, 263–270

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