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

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.

1995 ◽  
Vol 269 (1) ◽  
pp. E85-E90 ◽  
Author(s):  
J. Vanecek ◽  
D. C. Klein

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.


1994 ◽  
Vol 130 (5) ◽  
pp. 530-539 ◽  
Author(s):  
Wilfried Allaerts ◽  
Ans MI Tijssen ◽  
Pieter HM Jeucken ◽  
Hemmo A Drexhage ◽  
Jurrien de Koning

Allaerts W, Tijssen AMI, Jeucken PHM, Drexhage HA, de Koning J. Influence of folliculo-stellate cells on biphasic luteinizing hormone secretion response to gonadotropin-releasing hormone in rat pituitary cell aggregates. Eur J Endocrinol 1994;130:530–9. ISSN 0804–4643 Anterior pituitary cells cultured as three-dimensional cell aggregates and incubated with gonadotropin-releasing hormone (GnRH) show a biphasic pattern of luteinizing hormone (LH) release when steroid-free bovine follicle fluid is added to the culture medium. Initially, the GnRH-induced LH release is low (lag-phase response), but LH release increases during further incubations with GnRH (primed-state response). Also, in aggregates of dispersed cells from long-term ovariectomized rats cultured for 2 days in the presence of 1% bovine follicle fluid, a low initial LH responsiveness to GnRH could be restored. Cycloheximide was found to block the induction of the primed state, indicating the protein synthesis dependency of GnRH self-priming. In aggregates from gonadotroph-enriched cell populations obtained by velocity sedimentation in a bovine serum albumin gradient, addition of 1% bovine follicle fluid to the culture medium also restored a biphasic pattern of GnRH-induced LH release. However, co-culturing the gonadotroph-enriched cell aggregates with a folliculo-stellate (FS) cell-enriched population resulted in the attenuation of the differences in LH secretion rate between early and late responses to GnRH. The present example of the attenuation by folliculo-stellate cells of pituitary hormone secretion responses demonstrates that the cells regulate the cellular processes leading to a priming of the LH response to GnRH, rather than interfering with the access of GnRH to its receptor in gonadotrophs. Finally, it was found that stimulation of the adenylate cyclase enzyme with maximal effective doses of forskolin counteracted the inhibitory effect of bovine follicle fluid on the initial LH response to GnRH, but did not completely abolish the biphasic pattern of LH release. It is concluded that coupling to the adenylate cyclase enzyme is presumably involved in the LH surge inhibiting feedback action on the pituitary cells, but also other messenger pathways and intercellular interactions between pituitary cells may play a role in establishing a biphasic LH release at the pituitary level following GnRH administration. W Allaerts, Dept. of Immunology, Erasmus University Rotterdam, PO Box 1738, 3000 DR Rotterdam, The Netherlands


1988 ◽  
Vol 254 (5) ◽  
pp. E595-E600 ◽  
Author(s):  
D. E. Suter ◽  
N. B. Schwartz ◽  
S. J. Ringstrom

To verify the inhibitory effect of cortisol (F) on secretion of luteinizing hormone (LH) 24 h postorchidectomy, we implanted cholesterol (C) or F subcutaneously into male rats, and 4 days later orchidectomized or sham orchidectomized them under ether anesthesia. We injected gonadotropin-releasing hormone (GnRH) or saline into these rats 24 h postorchidectomy, collected blood 30 min later, and measured LH and follicle-stimulating hormone (FSH) in serum and pituitaries. F inhibited GnRH-induced secretion of LH without affecting secretion of FSH. We then implanted C, corticosterone (B), or F into rats, performed the same surgeries, and collected pituitaries 24 h after surgery for quantitation of receptors for GnRH. Neither F nor B affected the number of receptors for GnRH or their affinity for a GnRH analogue. Suppression of LH in serum occurred without decreased pituitary content of LH. In contrast, F increased pituitary content of FSH. Implantation of progesterone in a similar experiment did not affect circulating concentrations or pituitary contents of FSH or LH. These data suggest that glucocorticoids may inhibit responsiveness to GnRH by some mechanism distal to the receptor for GnRH that affects only LH.


1996 ◽  
Vol 135 (4) ◽  
pp. 455-463 ◽  
Author(s):  
Hadas Lewy ◽  
Zvi Naor ◽  
Israel E Ashkenazi

Lewy H, Naor Z, Ashkenazi IE. Rhythmicity of luteinizing hormone secretion expressed in vitro. Eur J Endocrinol 1996;135:455–63. ISSN 0804–4643 In the present study we explored the possibility that the pituitary functions as an autonomous clock and is capable of generating rhythms of luteinizing hormone (LH) release independently of hypothalamic control. Pituitaries from estrous or diestrous day 1 female mice were perifused separately with Medium-199. Effluent samples were collected at 10-min intervals and assayed for LH levels. Fourier analysis and curve-fit analysis served to elucidate the presence of prominent periods whose significance was then determined by best-fit cosinor. The latter method was used to determine additional parameters for the significant rhythm. All perifused pituitaries exhibited LH release patterns that were composed of significantly long ultradian rhythms (approximately 16 and 8 h, p < 0.001). Continuous stimulation with gonadotropin-releasing hormone (GnRH) or estradiol did not alter the periods of the observed rhythms but affected other rhythm parameters. Gonadotropin-releasing hormone increased the mesor of the rhythm and estradiol increased the amplitude. The results indicate that pituitary gonadotropes are capable of producing rhythms of LH release for a long duration in vitro, in the absence of hypothalamic control. Both GnRH and estradiol affect different rhythm parameters but do not change the periods of these rhythms. Israel E Ashkenazi, Department of Human Genetics, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel


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