Gonadotrophin release by gonadotrophs incubated with gonadotrophin-releasing hormone is independent of intracellular cAMP accumulation

1981 ◽  
Vol 97 (3) ◽  
pp. 329-337 ◽  
Author(s):  
L. Benoist ◽  
M. Le Dafniet ◽  
W. H. Rotsztejn ◽  
J. Besson ◽  
j. Duval
Keyword(s):  
Secondary Process ◽  
Intracellular Camp ◽  
Pituitary Cells ◽  
Camp Accumulation ◽  
Camp Content ◽  
Releasing Hormone ◽  
Rat Pituitary ◽  
Gonadotrophin Releasing Hormone ◽  
Rat Pituitary Cells ◽  
Intracellular Camp Accumulation

Abstract. Rat pituitary cells were dispersed with trypsin and separated by sedimentation at unit gravity. The distributions of prolactin (Prl), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) were determined, and two enriched cell populations (mammotrophs and gonadotrophs) were subsequently cultured. During a 4 h incubation, gonadotrophin-releasing hormone (GnRH) stimulated the release of LH and of FSH by both the unfractionated population and the enriched gonadotrophs; the magnitude of this stimulation increased with the length of the pre-culture periods, and the amount of LH released into the medium correlated strongly with the amount of FSH, whatever the length of the pre-culture period. The cellular cAMP content was also enhanced during the 4 h incubation, but no correlation was found between the hormone release and the cAMP accumulation. Furthermore, during the first 30 min of incubation with GnRH there was no increase of cellular cAMP, whatever cell population used. We conclude that the gonadotrophin release was independent of the cAMP accumulation observed in pituitary cells several hours after stimulation by GnRH; consequently, the late increase in the nucleotide is suggested to be a non-specific secondary process.

Kinetics of gonadotrophin-releasing hormone induced desensitization of rat pituitary cells.

1987 ◽  
Vol 116 (3_Suppl) ◽  
pp. S184-S185 ◽  
Author(s):  
K. J. HELM ◽  
L. KIESEL ◽  
T. RABE ◽  
B. RUNNEBAUM
Keyword(s):  
Pituitary Cells ◽  
Releasing Hormone ◽  
Rat Pituitary ◽  
Gonadotrophin Releasing Hormone ◽  
Rat Pituitary Cells ◽  
Kinetics Of

The effects of GH-releasing peptide-6 (GHRP-6) and GHRP-2 on intracellular adenosine 3′,5′-monophosphate (cAMP) levels and GH secretion in ovine and rat somatotrophs

1996 ◽  
Vol 148 (2) ◽  
pp. 197-205 ◽  
Author(s):  
D Wu ◽  
C Chen ◽  
J Zhang ◽  
C Y Bowers ◽  
I J Clarke
Keyword(s):  
Additive Effect ◽  
Intracellular Camp ◽  
Pituitary Cells ◽  
Dependent Manner ◽  
Camp Accumulation ◽  
Gh Secretion ◽  
Rat Pituitary ◽  
Rat Pituitary Cells ◽  
Camp Levels

Abstract The mechanism of action of GH-releasing peptide-6 (GHRP-6) and GHRP-2 on GH release was investigated in ovine and rat pituitary cells in vitro. In partially purified sheep somatotrophs, GHRP-2 and GH-releasing factor (GRF) increased intracellular cyclic AMP (cAMP) concentrations and caused GH release in a dose-dependent manner; GHRP-6 did not increase cAMP levels. An additive effect of maximal doses of GRF and GHRP-2 was observed in both cAMP and GH levels whereas combined GHRP-6 and GHRP-2 at maximal doses produced an additive effect on GH release only. Pretreatment of the cells with MDL 12,330A, an adenylyl cyclase inhibitor, prevented cAMP accumulation and the subsequent release of GH that was caused by either GHRP-2 or GRF. The cAMP antagonist, Rp-cAMP also blocked GH release in response to GHRP-2 and GRF. The cAMP antagonist did not prevent the effect of GHRP-6 on GH secretion whereas MDL 12,330A partially reduced the effect. An antagonist for the GRF receptor, [Ac-Tyr1,d-Arg2]-GRF 1–29, significantly diminished the effect of GHRP-2 and GRF on cAMP accumulation and GH release, but did not affect GH release induced by GHRP-6. Somatostatin prevented cAMP accumulation and GH release responses to GHRP-2, GRF and GHRP-6. Ca2+ channel blockade did not affect the cAMP increase in response to GHRP-2 or GRF but totally prevented GH release in response to GHRP-2, GRF and GHRP-6. These results indicated that GHRP-2 acts on ovine pituitary somatotrophs to increase cAMP concentration in a manner similar to that of GRF; this occurs even during the blockade of Ca2+ influx. GHRP-6 caused GH release without an increase in intracellular cAMP levels. GH release in response to all three secretagogues was reduced by somatostatin and was dependent upon the influx of extracellular Ca2+. The additive effect of GHRP-2 and GRF or GHRP-6 suggested that the three peptides may act on different receptors. In rat pituitary cell cultures, GHRP-6 had no effect on cAMP levels, but potentiated the effect of GRF on cAMP accumulation. The synergistic effect of GRF and GHRP-6 on cAMP accumulation did not occur in sheep somatotrophs. Whereas GHRP-2 caused cAMP accumulation in sheep somatotrophs, it did not do so in rat pituitary cells. These data indicate species differences in the response of pituitary somatotrophs to the GHRPs and this is probably due to different subtypes of GHRP receptor in rat or sheep. Journal of Endocrinology (1996) 148, 197–205

Short-term effects of oestradiol and 4-hydroxyoestradiol on gonadotrophin-releasing hormone induced luteinizing hormone secretion by rat pituitary cells in culture

1986 ◽  
Vol 111 (3) ◽  
pp. 312-320 ◽  
Author(s):  
G. Emons ◽  
O. Ortmann ◽  
U. Fingscheidt ◽  
P. Ball ◽  
R. Knuppen
Keyword(s):  
Hormone Secretion ◽  
Female Rats ◽  
Pituitary Cells ◽  
Luteinizing Hormone Secretion ◽  
Releasing Hormone ◽  
Rat Pituitary ◽  
The Media ◽  
Gonadotrophin Releasing Hormone ◽  
Rat Pituitary Cells ◽  
Sensitizing Effect

Abstract. Dispersed pituitary cells from adult female rats were preincubated for different time periods (0– 12 h) in the absence or presence of 10−9 moestradiol (E2) or 4-hydroxyoestradiol (4-OHE2). Then the media were changed and the cells incubated for 4 h with either vehicle, or E2, or 4-OHE2 and additionally with different concentrations (10−11– 10−7 m) of gonadotrophin-releasing hormone (GnRH). Treatment of pituitary cells with E2 for 4 h (i.e. no preincubation with E2) significantly decreased the LH-response to GnRH at concentrations ≥ 10−10 m of the decapeptide. During a transition time of approximately 10 h (i.e. in cultures preincubated with E2 or vehicle for 2, 4, 6 or 8 h and then coincubated with E2 or vehicle and GnRH for 4 h) no differences between E2-and vehicle-treated cultures were observed. After 14 and 16 h of E2-treatment (i.e. 10 or 12 h preincubation and 4 h coincubation with GnRH) the LH-responses to GnRH in these cultures were significantly higher than in the respective controls. A nearly identical reaction pattern was observed when 4-OHE2 was used instead of E2. In a second series of experiments dispersed rat pituitary cells were suspended in a carrier gel and continuously perifused with medium, using small chromatography columns. When these cells were exposed for 4 min to 10−9 m GnRH at 60 or 48 min intervals, they reacted with reproducible pulsatile LH-discharges during at least 6 subsequent stimuli with the decapeptide. When E2 (10−9 m) was added to the perifusion medium, the LH-responses to GnRH were significantly reduced, starting 36 min after the onset of E2-treatment. These data indicate: 1) In the rat, the negative oestrogen effect is at least in part directly mediated at the pituitary level. 2) The sensitizing effect of oestrogens on rat gonadotrophs to GnRH is significant already after 14 to 16 h. 3) E2 and the catecholoestrogen 4-OHE2 have the same effects in this system. 4) The negative E2-effect on GnRH-induced LH-release is significant after only 36 min, a finding bringing up the question of a non-genomic mechanism.

Melatonin inhibits luteinizing hormone releasing hormone (LHRH) induction of LH release from fetal rat pituitary cells

1995 ◽  
Vol 184 (2) ◽  
pp. 109-112 ◽  
Author(s):  
Atsuhiko Hattori ◽  
Damon C. Herbert ◽  
Mary K. Vaughan ◽  
Ken Yaga ◽  
Russel J. Reiter
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Cells ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Fetal Rat ◽  
Rat Pituitary ◽  
Lh Release ◽  
Rat Pituitary Cells

Modulatory effect of steroid hormones on GnRH-induced LH secretion by cultured rat pituitary cells

1992 ◽  
Vol 70 (7) ◽  
pp. 963-969 ◽  
Author(s):  
Gabriela T. Pérez ◽  
Marta E. Apfelbaum
Keyword(s):  
Steroid Hormones ◽  
Pituitary Cells ◽  
Short Term ◽  
Stimulatory Action ◽  
Rat Pituitary ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Rat Pituitary Cells ◽  
Lh Secretion

The purpose of the present experiments was to examine the short- and long-term effects of estradiol-17β (E2), progesterone (P), and 5α-dihydrotestosterone (DHT), alone and in combination, on the gonadotrophin-releasing hormone (GnRH)-induced luteinizing hormone (LH) secretion, using an ovariectomized rat pituitary cells culture model. After 72 h in steroid-free medium, pituitary cells were further cultured for 24 h in medium with or without E2 (1 nM), P (100 nM), or DHT (10 nM). Cultures were then incubated for 5 h in the absence or presence of 1 nM GnRH with or without steroids. LH was measured in the medium and cell extract by radioimmunoassay. The results show that the steroid hormones exert opposite effects on the release of LH induced by GnRH, which seems to be dependent upon the length of time the pituitary cells have been exposed to the steroids. In fact, short-term (5 h) action of E2 resulted in a partial inhibition (64% of control) of LH release in response to GnRH, while long-term (24 h) exposure enhanced (158%) GnRH-induced LH release. Similar results were obtained with DHT, although the magnitude of the effect was lower than with E2. Conversely, P caused an acute stimulatory action (118%) on the LH released in response to GnRH and a slightly inhibitory effect (90%) after chronic treatment. GnRH-stimulated LH biosynthesis was also influenced by steroid treatment. Significant increases in total (cells plus medium) LH were observed in pituitary cells treated with E2 or DHT. While the stimulatory effect of E2 was evident after both acute (133%) and chronic (119%) treatment, that of DHT appears to be exerted mainly after long-term priming (118%). These results suggest that the steroids modulate GnRH-induced LH secretion by acting on both synthesis and release of LH. On the other hand, total hormone content was not affected by P. The acute (5 h) effects of E2, P, and DHT on the GnRH response in E2-primed (24 h) cells during a short-term incubation, were also tested. Addition of P to the pituitary cells primed with E2 led to an acute potentiation of the stimulatory effect of E2 on GnRH-induced LH release and total content. Conversely, the augmentative E2 effect on pituitary responsiveness to GnRH was abolished by DHT. Taken together, these findings suggest that the physiological significance of the stimulatory action of progesterone could be to define the final magnitude of the LH preovulatory surge, while the inhibition by DHT could be required to limit the LH surge to that day of proestrus.Key words: luteinizing hormone, gonadotrophin-releasing hormone, steroid hormones, cultured pituitary cells.

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