Changes in the granule population of gonadotrophs of hypogonadal (hpg) and normal female mice associated with the priming effect of LH-releasing hormone in vitro

1986 ◽  
Vol 109 (1) ◽  
pp. 35-NP ◽  
Author(s):  
C. E. Lewis ◽  
J. F. Morris ◽  
G. Fink ◽  
M. Johnson
Keyword(s):  
Priming Effect ◽  
Marginal Zone ◽  
Secretory Granules ◽  
Initial Exposure ◽  
Releasing Hormone ◽  
Female Mice ◽  
Mean Diameter ◽  
Lh Release ◽  
The Mean ◽  
Lh Releasing Hormone

ABSTRACT Changes in the size and position of secretory granules in pituitary gonadotrophs have been studied in relationship to LH release and self-priming induced by LH-releasing hormone (LHRH) in pituitary glands from normal and hypogonadal (hpg) female mice. Hemipituitary glands were preincubated and then incubated for either 1 or 2 h in the absence or presence of LHRH (8·5 nmol/l). The glands were either processed for ultrastructural morphometry or homogenized for the determination of pituitary LH content. Morphometry was carried out on gonadotrophs identified by immunocytochemistry for LHβ using the thin/semi-thin section method. Pituitary LH content and the amount of LH released were determined by radioimmunoassay. The amount of LH released in response to the first and second hours of incubation with LHRH were similar in hpg and normal mice with a clear priming effect (three- to fourfold increase in pituitary responsiveness to LHRH) occurring in both strains. Despite a substantially reduced total number of granules (and amount of LH) in unstimulated hpg gonadotrophs, the number of granules in the outer 500 nm marginal zone of the cells was similar to that in normal mice. This could explain the similar amount of LH released from normal and hpg glands by the first LHRH challenge. The initial exposure to LHRH was also associated with a marked translocation of secretory granules from the central to the outer marginal region of cytoplasm subjacent to the gonadotroph plasmalemma, such that in 'primed' glands 60% of granules were found in this marginal zone compared with 40% (hpg) or 33% (normal) in unstimulated glands. The mean diameter of granules in the marginal zone was significantly less than that of granules in the central zone of the gonadotrophs of unstimulated glands from both normal and hpg animals. Exposure to LHRH for 1 h was associated with an increase in the number of small granules in the marginal zone and a significant decrease in the mean diameter of the gonadotroph granule population as a whole. After the primed release of LH, increased proportions of granules were still located in the marginal zone of gonadotrophs, indicating that granule migration continued during the second hour of exposure to LHRH in which primed release occurred. The primed release was associated with a detectable reduction in both the LH and granule content of gonadotrophs in normal, but not hpg glands. The ultrastructural correlates of LH release and LHRH priming were similar in the two strains of mice, and therefore in mice neither the releasing nor the priming effect of LHRH depends upon previous exposure of the pituitary gland to LHRH or ovarian factors. The priming effect was associated with a marked shift of granules towards the plasmalemma and a decrease in granule size which most likely resulted from increased post-translational processing within secretory granules. J. Endocr. (1986) 109, 35–44

Estradiol stimulation of LH response to LHRH and LHRH binding in pituitary cultures

1982 ◽  
Vol 242 (6) ◽  
pp. E392-E397
Author(s):  
L. K. Tang ◽  
A. C. Martellock ◽  
J. K. Horiuchi
Keyword(s):  
Cell Proliferation ◽  
Luteinizing Hormone ◽  
Priming Effect ◽  
Cultured Cells ◽  
Female Rats ◽  
Releasing Hormone ◽  
Lh Release ◽  
Estradiol Stimulation ◽  
Lh Releasing Hormone ◽  
Stimulation Of

The relationship between 17 beta-estradiol (E2) stimulation of luteinizing hormone (LH) response to LH-releasing hormone (LHRH) and E2 effect on LHRH binding was examined in pituitary monolayer cultures prepared from female rats. E2 pretreatment significantly (P less than 0.05) augmented the LHRH-induced LH release to 158-180% of the non-E2-treated controls. The maximal E2-priming effect could be observed after 1 day of treatment. E2 treatment for 3 days stimulated [D-Ala6]luteinizing hormone-releasing hormone (LHRHa) binding to about 1.5-fold that of the non-E2-treated controls without affecting the dissociation constant of LHRH receptor (Kd = 4 X 10(-10) M). The stimulatory effect of E2 on cell proliferation as determined by [3H]thymidine incorporation was also observed 3 days after treatment. However, E2 stimulation of LH accumulation in the cultured cells could be detected as early as 4 h after treatment. These results indicate that E2-priming effect on pituitary LH response to LHRH is initially associated with an increase in cellular LH content and later associated with increases in LHRH binding and in an index of cell proliferation that may include the LH-producing cells.

The role of microfilaments in the priming effect of LH-releasing hormone: an ultrastructural study using cytochalasin B

1985 ◽  
Vol 106 (2) ◽  
pp. 211-NP ◽  
Author(s):  
C. E. Lewis ◽  
J. F. Morris ◽  
G. Fink
Keyword(s):  
Adult Female ◽  
Ultrastructural Study ◽  
Incubation Medium ◽  
Priming Effect ◽  
Cytochalasin B ◽  
Secretory Granules ◽  
Releasing Hormone ◽  
Lh Releasing Hormone ◽  
Lh Secretion

ABSTRACT We have investigated the possibility that microfilaments are involved in the priming effect of LH-releasing hormone (LHRH) by ultrastructural morphometry of hemipituitary glands from adult female mice. Glands incubated for 2 consecutive hours with 8·5 nmol LHRH/1 responded with a marked increase in the amount of LH released into the medium during the second hour compared with the first hour of incubation. This priming effect of LHRH on LH secretion was accompanied by a significant margination of secretory granules and a drop in the total granule content of the gonadotrophs. Although the number of microfilaments remained the same, there was an increase in their length and a change in orientation so that the angle between the microfilaments and the plasmalemma was significantly reduced after both the first and second hour of exposure of LHRH. The addition of 14·3 μmol cytochalasin B/l to the incubation medium significantly increased the amount of LH released in the first hour of incubation when compared with the amount of LH released by LHRH alone, but completely abolished the priming effect of LHRH. Cytochalasin B also prevented the LHRH-induced increase in the length and the change in orientation of the microfilaments. These results indicate that LHRH priming involves an increase in length of microfilaments and a change in their orientation relative to the plasmalemma. J. Endocr. (1985) 106, 211–218

Kinetic evidence for two components in the priming effect of LH-releasing hormone in the rat

1991 ◽  
Vol 129 (3) ◽  
pp. 351-355 ◽  
Author(s):  
M. S. Johnson ◽  
R. Mitchell
Keyword(s):  
Priming Effect ◽  
Maximum Amount ◽  
Response Curves ◽  
Initial Exposure ◽  
Low Concentrations ◽  
Before And After ◽  
Lh Release ◽  
Stimulus Secretion Coupling ◽  
Lh Releasing Hormone

ABSTRACT The priming effect of LHRH on LH release from prooestrous rat hemipituitary glands in vitro was analysed by kinetic approaches. Concentration–response curves for LHRH-, K+- and ionomycin-induced LH release were constructed for initial exposure to the secretagogues and after 'priming' with a low dose of LHRH (100 pg/ml). These data were analysed by a non-linear curve-fitting programme to reveal the potency and maxima of the responses before and after priming. The parameters obtained from the curves fitted to the LHRH concentration–response curves showed that two changes had occurred as a result of priming. There was an increase in the maximum amount of hormone released and also a relatively greater ability for low concentrations of LHRH to cause release (increased potency). The data for K+ and ionomycin revealed only one change as a result of priming, an increase in the maximum amount of hormone available for release. The data indicate that LHRH, after self-priming, releases more hormone by at least two routes, one represented by a general increase in stimulus–secretion coupling (which is available to K+ and ionomycin), the other a specific up-regulation of signal transduction by the LHRH receptor–effector system. Journal of Endocrinology (1991) 129, 351–355

RESTORATION OF OESTROGEN POSITIVE FEEDBACK EFFECT ON LH RELEASE BY BROMOCRIPTINE IN HYPERPROLACTINAEMIC PATIENTS WITH GALACTORRHOEA-AMENORRHOEA

1979 ◽  
Vol 91 (3) ◽  
pp. 591-600 ◽  
Author(s):  
Toshihiro Aono ◽  
Akira Miyake ◽  
Takenori Shioji Motoi Yasuda ◽  
Koji Koike ◽  
Keiichi Kurachi
Keyword(s):  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Serum Prolactin ◽  
Serum Luteinizing Hormone ◽  
Serum Lh ◽  
Lh Release ◽  
The Mean ◽  
Lh Rh ◽  
Lh Releasing Hormone ◽  
Positive Feedback Effect

ABSTRACT Five mg of bromocriptine was administered for 3 weeks to 8 hyperprolactinaemic women with galactorrhoea-amernorrhoea, in whom the response of serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) to 100 μg of iv LH-releasing hormone (LH-RH) had been evaluated. Twenty mg of conjugated oestrogen (Premarin®) was injected iv any day between the 10th and 12th day from the initiation of the treatment, and serum LH levels were serially determined for 120 h. Hyperresponse of LH with normal FSH response to LH-RH was observed in most patients. Bromocriptine treatment for 10 to 12 days significantly suppressed mean (± se) serum prolactin (PRL) levels from 65.1 ± 23.0 to 10.4 ± 2.0 ng/ml, while LH (12.6 ± 2.1 to 24.8 ± 5.9 mIU/ml) and oestradiol (40.1 ± 7.6 to 111.4 ± 20.8 pg/ml) levels increased significantly. Patients on bromocriptine treatment showed LH release with a peak at 48 h after the injection of Premarin. The mean per cent increases in LH were significantly higher than those in untreated patients with galactorrhoea-amenorrhoea between 32 and 96 h after the injection. The present results seem to suggest that the restoration of LH-releasing response to oestrogen following suppression of PRL by bromocriptine may play an important role in induction of ovulation in hyperprolactinaemic patients with galactorrhoea-amenorrhoea.

Multiple injections of LH-releasing hormone into hypogonadal (hpg) mice induce the appearance of two morphologically distinct populations of gonadotrophs

1986 ◽  
Vol 111 (3) ◽  
pp. 483-NP ◽  
Author(s):  
C. E. Lewis ◽  
A. Megson ◽  
J. F. Morris ◽  
H. M. Charlton
Keyword(s):  
Lipid Droplets ◽  
Secretory Granules ◽  
Male And Female ◽  
Releasing Hormone ◽  
Multiple Injections ◽  
Adult Mice ◽  
Full Development ◽  
Free Cells ◽  
Pituitary Glands ◽  
Lh Releasing Hormone

ABSTRACT We have investigated the effects of multiple 2-hourly injections of LH-releasing hormone (LHRH) on the number and size of the gonadotrophs and gonadotroph secretory granules, and the lipid content of gonadotrophs in the pituitary glands of intact and gonadectomized male and female hypogonadal (hpg) mice. Gonadotrophs were identified by immunocytochemistry for LHβ, and the size and secretory status of the gonadotrophs were assessed by quantitative ultrastructural analysis of immunoidentified gonadotrophs. The administration of 60 ng LHRH by subcutaneous injection every 2 h for 15 days resulted in an increase in the number, size and granule content of LHβ-immunoidentified gonadotrophs of hpg mice to values found in normal adult mice. Large lipid droplets accumulated in 30–40% of the gonadotrophs in both male and female LHRH-treated hpg mice. Although lipid-containing gonadotrophs were larger than lipid-free cells in all LHRH-treated groups irrespective of the presence or absence of gonads, a marked difference in the number, position within the cell, and size of the secretory granules between the lipid-containing and lipid-free cells was found only in the pituitary glands of intact LHRH-treated hpg females. These results demonstrate: (a) that the effects of multiple injections of LHRH on the morphology of the gonadotrophs of hpg mice is not dependent on the presence of functioning gonads, although ovarian factors are required for the full development of morphological, and hence possibly functional, heterogeneity in the gonadotroph population in female animals, and (b) that, although multiple injections of LHRH in hpg mice are more effective than single daily injections of LHRH in stimulating pituitary-gonadal function, there is no obvious difference in the morphologically recognizable effects that these two modes of administration have on the pituitary gonadotrophs. J. Endocr. (1986) 111, 483–493

LH Release by LH-Releasing Hormone in Golden Hamsters at Various Stages of Estrous Cycle

1972 ◽  
Vol 140 (2) ◽  
pp. 609-612 ◽  
Author(s):  
A. Arimura ◽  
L. Debeljuk ◽  
A. V. Schally
Keyword(s):  
Estrous Cycle ◽  
Releasing Hormone ◽  
Golden Hamsters ◽  
Lh Release ◽  
Lh Releasing Hormone

Changes in pituitary responsiveness to LH-releasing hormone after acute buserelin treatment: a time-course and dose–response study

1985 ◽  
Vol 106 (1) ◽  
pp. 27-30 ◽  
Author(s):  
J. D. Heather ◽  
S. A. Whitehead
Keyword(s):  
Time Course ◽  
Dependent Manner ◽  
Releasing Hormone ◽  
Serum Lh ◽  
Significant Difference ◽  
Lh Release ◽  
Lh Releasing Hormone ◽  
In Vivo Effects ◽  
Dose Response Study

ABSTRACT The acute in-vivo effects of a potent LH-releasing hormone (LHRH) agonist, buserelin, on LH secretion and pituitary responsiveness to LHRH have been investigated in oestrous rats. Doses of 50, 100 and 250 ng buserelin stimulated LH release in a dose-dependent manner, the peak serum LH concentrations being measured 1 h after the treatment. Thereafter LH levels fell rapidly between 1 and 6 h and by 18 h serum LH concentrations were similar in all groups of animals. Pituitary responsiveness to a challenge with 100 ng LHRH was potentiated by 50 or 100 ng buserelin injected 1 or 2 h before the LHRH challenge. In contrast, 250 ng buserelin completely abolished the LH response to LHRH when tested 1, 2 and 4 h after treatment, but by 6 h a small but attenuated response was observed. Four hours after treatment there was no significant difference in the responses when compared with the saline-treated controls. J. Endocr. (1985) 106, 27–30

Pituitary and testicular responses in sexually mature bulls after intravenous injections of graded doses of LH-releasing hormone

1984 ◽  
Vol 103 (3) ◽  
pp. 371-376 ◽  
Author(s):  
M. J. D'Occhio ◽  
B. P. Setchell
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Anterior Pituitary Gland ◽  
Limiting Factor ◽  
Releasing Hormone ◽  
Intravenous Injections ◽  
Gonadotrophin Secretion ◽  
Lh Release ◽  
Lh Releasing Hormone ◽  
Sexually Mature

ABSTRACT The capacity of the anterior pituitary gland and testes in mature bulls (705±9 (s.e.m.) kg body wt, n = 4) to respond to graded doses of LH-releasing hormone (LHRH) was assessed relative to endogenous profiles of LH and testosterone secretion. Endogenous hormone profiles were determined by bleeding bulls at 20-min intervals for 12 h. Responses to LHRH were assessed on successive days after single intravenous injections of 1, 5, 10, 50 or 100 ng LHRH/kg body wt. Blood samples were taken at −40, −20, 0, 10, 20, 30, 40, 60 and 120 min relative to LHRH injection. During a 12-h bleed bulls showed spontaneous pulses of LH and testosterone which had peak amplitudes of 2·6±0·5 μg/l and 44·5 ± 7·1 nmol/l respectively. Respective peak LH (μg/l) and testosterone (nmol/l) responses to LVRH were as follows: 1 ng LHRH (3·0±0·7: 47·3±4·1); 5 ng LHRH (8·0±1·2; 52·8 ± 6·2); 10 ng LHRH (11·1±2·3; 57·7 ± 9·1); 50 ng LHRH (19·2±2·8; 47·9±8·6); 100 ng LHRH (19·1±4·7; 43·9 ±6·4). A dose of 1 ng LHRH/kg produced LH and testosterone responses which were comparable in amplitude to spontaneous peaks in the respective hormone. There was a linear (y = 0·28x+5·72; r = 0·81) increase in the LH response to doses of LVRH between 1 and 50 ng/kg; corresponding testosterone responses showed no relationship with the dose of LHRH. The capacity of the anterior pituitary gland to release amounts of LH eight to ten times in excess of those secreted during spontaneous peaks suggests that (1) there exists a large releasable store of LH in the anterior pituitary gland and (2) hypothalamic LHRH is a limiting factor in gonadotrophin secretion. In contrast to LH release, the androgenic response of the testes to acute gonadotrophic stimulation is determined largely by prevailing steroidogenic activity. J. Endocr. (1984) 103, 371–376

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.

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