A Model System for the Study of Luteinizing Hormone (LH) Secretion: Lack of Effect of Fetal Calf Serum on Gonadotropin-Releasing Hormone Stimulated LH Release

1982 ◽  
Vol 170 (1) ◽  
pp. 82-88 ◽  
Author(s):  
J. L. C. Borges ◽  
D. L. Kaiser ◽  
W. S. Evans ◽  
M. O. Thorner
Keyword(s):  
Luteinizing Hormone ◽  
Fetal Calf Serum ◽  
Calf Serum ◽  
Model System ◽  
Gonadotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Release ◽  
Lh Secretion

scholarly journals Induction of final oocyte maturation in Cyprinidae fish by hypothalamic factors: a review

2009 ◽  
Vol 54 (No. 3) ◽  
pp. 97-110 ◽  
Author(s):  
P. Podhorec ◽  
J. Kouril
Keyword(s):  
Luteinizing Hormone ◽  
Oocyte Maturation ◽  
Hormone Secretion ◽  
Inhibitory Effect ◽  
Gonadotropin Releasing Hormone ◽  
Luteinizing Hormone Secretion ◽  
Releasing Hormone ◽  
Final Oocyte Maturation ◽  
In Captivity ◽  
Lh Secretion

Gonadotropin-releasing hormone in Cyprinidae as in other Vertebrates functions as a brain signal which stimulates the secretion of luteinizing hormone from the pituitary gland. Two forms of gonadotropin-releasing hormone have been identified in cyprinids, chicken gonadotropin-releasing hormone II and salmon gonadotropin-releasing hormone. Hypohysiotropic functions are fulfilled mainly by salmon gonadotropin-releasing hormone. The only known factor having an inhibitory effect on LH secretion in the family Cyprinidae is dopamine. Most cyprinids reared under controlled conditions exhibit signs of reproductive dysfunction, which is manifested in the failure to undergo final oocyte maturation and ovulation. In captivity a disruption of endogenous gonadotropin-releasing hormone stimulation occurs and sequentially that of luteinizing hormone, which is indispensible for the final phases of gametogenesis. In addition to methods based on the application of exogenous gonadotropins, the usage of a method functioning on the basis of hypothalamic control of final oocyte maturation and ovulation has become popular recently. The replacement of natural gonadotropin-releasing hormones with chemically synthesized gonadotropin-releasing hormone analogues characterized by amino acid substitutions at positions sensitive to enzymatic degradation has resulted in a centuple increase in the effectiveness of luteinizing hormone secretion induction. Combining gonadotropin-releasing hormone analogues with Dopamine inhibitory factors have made it possible to develop an extremely effective agent, which is necessary for the successful artificial reproduction of cyprinids.

Melatonin inhibition of GnRH-induced LH release from neonatal rat gonadotroph: involvement of Ca2+ not cAMP

1995 ◽  
Vol 269 (1) ◽  
pp. E85-E90 ◽  
Author(s):  
J. Vanecek ◽  
D. C. Klein
Keyword(s):  
Luteinizing Hormone ◽  
Second Messenger ◽  
Gonadotropin Releasing Hormone ◽  
Neonatal Rat ◽  
Dibutyryl Camp ◽  
Releasing Hormone ◽  
Cyclic Monophosphate ◽  
Lh Release

Melatonin inhibits gonadotropin-releasing hormone-induced release of luteinizing hormone (LH) from the neonatal rat gonadotrophs. The second messenger involved is not known, although there are several candidates, including adenosine 3',5'-cyclic monophosphate (cAMP) and intracellular free Ca2+. The present study addresses the question of which second messenger mediates melatonin inhibition of LH release. We found that the effect of melatonin was not prevented by cAMP protagonists, including 8-bromo-cAMP, dibutyryl cAMP, 3-isobutyl-1-methylxanthine, and forskolin. However, treatments that enhanced Ca2+ influx masked the effects of melatonin, and treatments that blocked Ca2+ influx mimicked the effects of melatonin. Moreover, melatonin decreased K(+)-induced LH release, which is dependent on Ca2+ influx but did not block release of LH due to thapsigargin-induced mobilization of Ca2+ from intracellular stores. These findings indicate that melatonin inhibits gonadotropin-releasing hormone-induced LH release, primarily through an action involving inhibition of Ca2+ influx, and that cAMP does not seem to be involved in this effect of melatonin.

Control of follicle-stimulating hormone secretion by steroid-free bovine follicular fluid in the ovariectomized rat

1983 ◽  
Vol 99 (1) ◽  
pp. 1-8 ◽  
Author(s):  
T. R. Koiter ◽  
G. C. J. van der Schaaf-Verdonk ◽  
H. Kuiper ◽  
N. Pols-Valkhof ◽  
G. A. Schuiling
Keyword(s):  
Luteinizing Hormone ◽  
Follicular Fluid ◽  
Hormone Secretion ◽  
Ovariectomized Rats ◽  
Ovariectomized Rat ◽  
Releasing Hormone ◽  
Basal Release ◽  
Lh Release ◽  
Lh Releasing Hormone ◽  
Lh Secretion

The effects of steroid-free bovine follicular fluid (bFF) and sodium phenobarbitone on spontaneous LH releasing hormone (LHRH)-induced secretion of FSH and LH were studied in ovariectomized rats. Luteinizing hormone releasing hormone was administered by infusion to rats anaesthetized with phenobarbitone. Bovine follicular fluid reduced FSH release and synthesis. Luteinizing hormone release remained unaffected after bFF treatment. Phenobarbitone reduced both FSH and LH release. The observed suppressive effects of bFF and phenobarbitone on FSH secretion were additive, suggesting that the basal release of FSH has an LHRH-dependent and an LHRH-independent component. Furthermore, bFF did not affect pituitary responsiveness of LH secretion to LHRH and reduced the responsiveness of FSH secretion only when administered some time before the LHRH challenge. The present observations support the view that in the ovariectomized rat the pituitary gland is the only site of action of inhibin-like activity as present in bFF.

RELEASE OF LH FOLLOWING INTRAUTERINE ADMINISTRATION GONADOTROPIN-RELEASING HORMONE

1980 ◽  
Vol 60 (4) ◽  
pp. 1023-1026 ◽  
Author(s):  
J. G. MANNS ◽  
W. D. HUMPHREY ◽  
B. MURPHY ◽  
B. BURTON
Keyword(s):  
Luteinizing Hormone ◽  
Gonadotropin Releasing Hormone ◽  
Gnrh Analogue ◽  
Releasing Hormone ◽  
Lh Release

Gonadotropin-releasing hormone (GnRH, 100 μg) or a potent analogue (50 μg) were administered into the uterus of proestrous cows (n = 6) in 0.5 mL of saline or semen diluent. GnRH analogue, but not GnRH, caused pituitary luteinizing hormone (LH) release which lasted approximately 4 h and reached maximum concentrations of 40–100 ng/mL by 2 h after treatment.

Functional Assessment of Intrahypothalamic Implants of Immortalized Gonadotropin-Releasing Hormone-Secreting Cells in Female Hypogonadal Mice

1993 ◽  
Vol 2 (3) ◽  
pp. 251-257 ◽  
Author(s):  
Gregory M. Miller ◽  
Ann-Judith Silverman ◽  
James L. Roberts ◽  
Ke Wen Dong ◽  
Marie J. Gibson
Keyword(s):  
Functional Assessment ◽  
Piriform Cortex ◽  
Gonadotropin Releasing Hormone ◽  
Olfactory Tubercle ◽  
Secreting Cell ◽  
Pharmacological Agents ◽  
Releasing Hormone ◽  
Lh Release ◽  
Lh Secretion ◽  
Intravenous Catheters

The hypogonadal (HPG) mouse is a mutant that lacks a functional gonadotropin-releasing hormone (GnRH) gene. In this study, female HPG mice received bilateral intrahypothalamic implants of an immortalized GnRH-secreting cell line (GT1-7). Nine mice were tested 42-65 days after implantation to determine whether these cells could support spontaneous and/or N-methyl-D, L,-aspartic acid (NMDA)-stimulated luteinizing hormone (LH) secretion. When sampled via intravenous catheters, four mice had measurable LH secretion. Three of these mice responded to NMDA challenges with significant increases in circulating LH. GnRH immunocytochemistry revealed that GT1-7 cells were present in these four mice and three others in which LH values were not detectable. There were about 1200 GnRH cells dispersed within the piriform cortex and olfactory tubercle, and no tumor found in one of the HPG mice that responded to NMDA, whereas the other NMDA responders had large bilateral hypothalamic tumors. The presence or absence of such tumors did not predict the capacity to respond to the NMDA challenge with alterations in LH secretion. This study provides the first evidence that intrahypothalamic GT1-7 cells can support LH release in the HPG mouse, and that this secretion can be modified by pharmacological agents.

scholarly journals Effects of Central Injection of Anti-LPS Antibody and Blockade of TLR4 on GnRH/LH Secretion during Immunological Stress in Anestrous Ewes

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Karolina Haziak ◽  
Andrzej Przemysław Herman ◽  
Dorota Tomaszewska-Zaremba
Keyword(s):  
Luteinizing Hormone ◽  
Anterior Pituitary ◽  
Gonadotropin Releasing Hormone ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Immune Stress ◽  
Immunological Stress ◽  
Lh Release ◽  
Lh Secretion ◽  
Tlr4 Receptor

The present study was designed to examine the effect of intracerebroventricular (icv) administration of antilipopolysaccharide (LPS) antibody and blockade of Toll-like receptor 4 (TLR4) during immune stress induced by intravenous (iv) LPS injection on the gonadotropin-releasing hormone/luteinizing hormone (GnRH/LH) secretion in anestrous ewes. Injection of anti-LPS antibody and TLR4 blockade significantly (P < 0.01) reduced the LPS dependent lowering amount ofGnRHmRNA in the median eminence (ME). Moreover, blockade of TLR4 caused restoration ofLH-βtranscription in the anterior pituitary decreased by the immune stress. However, there was no effect of this treatment on reduced LH release. The results of our study showed that the blockade of TLR4 receptor in the hypothalamus is not sufficient to unblock the release of LH suppressed by the immune/inflammatory challenges. This suggests that during inflammation the LH secretion could be inhibited directly at the pituitary level by peripheral factors such as proinflammatory cytokines and circulating endotoxin as well.

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