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At least 1,315 records · Page 73Linked to original sources
PubMed1988

Pulsatile nature of luteinizing hormone release is maintained during luteinizing hormone-releasing hormone stimulation in normal male rats.

The plasma LH concentration is believed to be reasonably steady in normal male rats. We found that LH is released in a regular pulsatile fashion. The overall mean concentration of plasma LH in normal male rats was 46.6 +/- 4.4 (mean +/- SEM) ng/ml. The normal male rats showed periodic LH pulses: the mean pulse amplitude was 144.4 +/- 25.5 ng/ml and the inter-peak interval was 22.5 +/- 2.0 min. Each pulse lasted 9.7 +/- 0.8 min. When LH-RH (1 microgram/kg) was injected as a bolus, the peak concentration was attained in 10-30 min reaching a peak concentration of 279.4 +/- 39.6 ng/ml. Distinct pulsatile bursts of plasma LH were discernible during the period of elevated plasma LH concentration. When a higher dose of LH-RH (5 micrograms/kg) was administered, the LH concentration slowly increased to a peak concentration of 400.2 +/- 38.7 ng/ml in 20-40 min. The pulsatile nature of the LH concentration was recognizable with distinct bursts. We have observed that: (a) normal male rats release LH in a pulsatile fashion with an approximate 20-min inter-peak interval; (b) mean LH pulses last less than 10 min, and (c) the LH pulses are visible even with elevated LH and LH-RH concentrations in the general circulation.

Animals↗
PubMed1995

Growth-promoting actions of parathyroid hormone, adrenocorticotrophic hormone, and thyroid-stimulating hormone: in vitro studies in normal and pygmy T-lymphoblast cell lines.

We used an in vitro T-lymphoblast clonal proliferation assay to quantify human IGF-I (hIGF-I)-, human PTH (hPTH)-, human ACTH (hACTH)-, and human TSH (hTSH)-stimulated growth of human T-cell leukemia virus-II-transformed T-lymphoblast cell lines from normal individuals and to elucidate the role of IGF-I as the mediator of hPTH-, hACTH-, and hTSH-induced T-cell growth. Normal T-lymphoblast cell lines respond to hIGF-I in a bimodal fashion. The mean first peak response was 143 +/- 9.8% above baseline (defined as 100%) occurring at 8 micrograms/L, and the mean second peak response was 154 +/- 14.4% occurring at 100 micrograms/L. Both responses were completely blocked after incubation with alpha IR-3, an MAb to the IGF-I receptor (by analysis of variance, p = 0.015 between full response curves). After stimulation with hPTH, the mean peak clonal response of normal T-lymphoblast cell lines was 189 +/- 7.0%; after incubation with alpha IR-3, the mean peak clonal response was 108 +/- 7.9% (p = 0.0015 between full response curves). The mean peak clonal response of normal T-lymphoblast cell lines after hACTH stimulation was 192 +/- 8.6%; preincubation with alpha IR-3 reduced the mean peak clonal response to 94 +/- 1.2% (p < 0.0001 between full response curves). With hTSH stimulation, the mean peak clonal response of normal T-lymphoblast cell lines was 167 +/- 7.0%; after incubation with alpha IR-3, the mean peak clonal response was 94 +/- 8.2% (p = 0.003 between full response curves).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed2004

Extracellular signal-regulated kinase, Jun N-terminal kinase, p38, and c-Src are involved in gonadotropin-releasing hormone-stimulated activity of the glycoprotein hormone follicle-stimulating hormone beta-subunit promoter.

The role of ERK, Jun N-terminal kinase (JNK), p38, and c-Src in GnRH-stimulated FSHbeta-subunit promoter activity was examined in the LbetaT-2 gonadotroph cell line. Incubation of the cells with a GnRH agonist resulted in activation of ERK, JNK, p38, and c-Src. The peak of ERK activation was observed at 5 min, whereas that of JNK, p38, and c-Src at 30 min, declining thereafter. ERK activation by GnRH is dependent on protein kinase C (PKC), as evident by activation, inhibition, and depletion of 12-O-tetradecanoylphorbol-13-acetate-sensitive PKC subspecies. Ca(2+) influx, but not Ca(2+) mobilization, is required for ERK activation. GnRH signaling to ERK is partially mediated by dynamin and a protein tyrosine kinase, apparently c-Src. ERK activation by GnRH in LbetaT-2 cells does not involve transactivation of epidermal growth factor receptor or mediation via Gbetagamma or beta-arrestin. Once activated by GnRH, ERK translocates to the nucleus. We examined the role of ERK, JNK, p38, and c-Src in GnRH-stimulated ovine FSHbeta promoter, linked to a luciferase reporter gene (-4741oFSHbeta-LUC). The PKC activator 12-O-tetradecanoylphorbol-13-acetate, but not the Ca(2+) ionophore ionomycin, stimulated FSHbeta-luciferase (LUC) activity. Furthermore, down-regulation of PKC, but not removal of Ca(2+), inhibited the GnRH response. Cotransfection of FSHbeta-LUC and the constitutively active forms of Raf-1 and MEK stimulated FSHbeta-LUC activity, whereas the dominant negatives of Ras, Raf-1, and MEK and the selective MEK inhibitor PD98059, abolished GnRH-induced FSHbeta-LUC activity. The dominant negatives of CDC42 and JNK reduced the GnRH response by 36 and 49%, respectively. Incubation of the cells with the p38 or the c-Src inhibitors SB203580 and PP1 also reduced the GnRH response. Surprisingly, two proximal activator protein-1 sites contribute very little to the GnRH response. Thus, PKC, ERK, JNK, p38, and c-Src, but not Ca(2+), are involved in GnRH induction of the ovine FSHbeta gene.

Animals↗
PubMed1978

Studies on the subsynaptosomal localization of luteinizing hormone-releasing hormone and thyrotropin-releasing hormone in the rat hypothalamus.

In the current investigation, subcellular particles (synaptosomes) of hypothalamic homogenates were isolated by differential centrifugation and discontinuous sucrose density gradient fractionation and found to be rich in LHRH, TRH, and the neuronal marker, norepinephrine (NE). Of the total quantity of LHRH, TRH, or NE in the nuclei-free homogenate, 52-65% was recovered in synaptosomes, whereas the cytosol, myelin/microsomes, and mitochondria contained only 1-12%. To determine the subsynaptosomal localization of LHRH and TRH, purified synaptosomes were lysed and the resulting suspensions were fractionated on discontinuous sucrose density gradients. LHRH (30-40%) was found to be localized primarily in subsynaptosomal particles which banded at sucrose densities between 0.6-1.0 M. Electron micorscopic analysis of these particles revealed the presence of dense-cored granules (70-80 nm diameter) and synaptosomal membrane remnants. Norepinephrine was found in two pools within the isolated nerve endings: 15-25% of synaptosomal NE was associated with the synaptic vesicles (45-55-nm diameter); about 40% was in the cytosol. TRH was present primarily as a soluble component of the nerve ending. No apparent association of TRH with dense-cored granules was demonstrable in this study; however, there may be some TRH in synaptic vesicles.

Animals↗
PubMed1979

Development of glycoprotein hormones and their alpha- and beta-subunits in bovine fetal pituitary glands. I. Quantitation of thyrotropin, follicle-stimulating hormone, and luteinizing hormone by radioligand receptor assays.

The development of TSH, FSH, and LH in bovine fetal pituitary glands was studied by the respective radioligand receptor assays. The content of pituitary TSH increased gradually in fetuses of both sexes throughout gestation, and no significant difference was observed for the pituitary concentration of TSH between male and female fetuses at different stages of gestation. The pituitary content of FSH increased gradually in male fetuses, but increased dramatically in female fetuses after midgestation. Similarly, the concentration of pituitary FSH was 2- to 3-fold higher in female than male fetuses after midgestation. The pituitary content of LH increased gradually and proportionally with the age of the fetus, and no significant difference was observed between sexes. However, the concentration of pituitary LH remained relatively constant for both sexes throughout gestation.

Animals↗
PubMed1980

The effect of an antiserum to luteinizing hormone-releasing hormone on the progesterone-induced luteinizing hormone surge in ovariectomized, estrogen-primed rats.

A rabbit antiserum to synthetic LHRH was shown to be specific to rat hypothalamic LHRH, as revealed by binding studies (RIA). The present study was undertaken to determine the effects of this antiserum (LHRH-AS) on the progesterone-induced LH surge in ovariectomized rats primed with estrogen on the proestrous LH surge in cycling females. An ip injection of 0.2 ml LHRH-AS at 1200 h on proestrus completely inhibited the preovulatory rise in serum LH from 1700-1800 h. In long term ovariectomized rats, a sc injection of estradiol benzoate reduced serum LH levels by 50% at 1200 h on the third day. Subsequent administration of progesterone elicited a LH surge, with peak LH value 4-6 h after progesterone. However, concurrent administration of LHRH-AS effectively prevented the increase in LH release by progesterone, and an iv injection of LHRH-AS was shown to be more effective than ip administration in inhibiting the progesterone stimulation of LH release. Although estrogen and progesterone may induce a change in pituitary responsiveness to hypothalamic LHRH in ovariectomized rats, the present study provides evidence that tonic and/or increased LHRH release is required for the acute increase in LH release caused by progesterone.

Animals↗
PubMed1980

Action of cholera toxin on hormone synthesis and release in GH cells: evidence that adenosine 3',5'-monophosphate does not mediate the decrease in growth hormone synthesis caused by thyrotropin-releasing hormone.

We have examined the effects of cholera toxin, a specific probe for processes which are caused by an increase in cAMP, on clonal strains of rat pituitary cells (GH cells) in culture. We found that 5 ng/ml cholera toxin increased the amount of intracellular cAMP after a lag period of 30-60 min. After a similar lag period, cholera toxin increased the release of PRL into the medium by 50% and caused a decrease in intracellular PRL to 60% of control values at 90 min. PRL synthesis was increased to 100% above control after 1 week of treatment, and GH synthesis was elevated to 280% above control. TRH caused an increase in PRL release and synthesis but a decrease of GH synthesis. Depending on the dose, TRH prevented or reduced the cholera toxin-induced rise in GH synthesis. We conclude that the decrease in GH synthesis caused by TRH is not likely to be mediated through an increase of intracellular cAMP.

Animals↗
PubMed1981

Differential effects of luteinizing hormone-releasing hormone on follicle-stimulating hormone-dependent responses in rat granulosa cells and Sertoli cells in vitro.

The abilities of LHRH and a potent LHRH agonist ([D-Ser-(But),6, des-Gly-NH210]LHRH ethylamide) inhibit FSH responses by rat granulosa cells and Sertoli cells in vitro have been compared. Granulosa cells isolated from 22- or 25-day-old diethylstilbestrol-primed rats and cultured under defined conditions for 48 h with NIH-FSH-S13 (300 ng/ml) or cholera toxin (0.1 microgram/ml) showed increased aromatase activity, as determined by the release of 3H2O from [1 beta-3H]testosterone. LHRH (10(-7) M) or th agonist (10(-8) M) added simultaneously with FSH or cholera toxin inhibited the effects on the release of 3H2O without influencing the protein content of the cell cultures. A smaller stimulation of 3H2O production occurred with (Bu)2cAMP (1.0 mM) plus 3-isobutyl-l-methylxanthine (0.1 mM), and this was partially suppressed in the presence of LHRH or the agonist. Parallel studies with Sertoli cells from 15- or 20-day-old rats demonstrated that culture under appropriate conditions with FSH, cholera toxin, or (Bu)2cAMP (0.5 mM) for 24 h caused an increase in cellular aromatase activity and enhanced secretion into the medium of plasminogen activator. However, no inhibition by LHRH (10(-7) or 10(-9) M) or the agonist (10(-6) or 10(-8) M) occurred when the peptides were added either simultaneously or 24 h before the stimulatory agent. Similarly, Sertoli cells from 11-day-old rats treated daily with LHRH agonist for 5 days in culture, showed no inhibition of aromatase activity after a 4-h stimulation with FSH or (Bu)2cAMP. FSH dose-response curves (0-300 ng/ml) for aromatase activity were shown to be similar after 5 days of culture with or without 10(-8) M LHRH agonist, indicating that the LHRH did not cause a shift in the sensitivity to FSH. The lack of inhibition was seen in Sertoli cell cultures maintained at 37 or 32 C. The enzyme digestion method used to isolated Sertoli cells was not responsible for the lack of effects of LHRH, since cell cultures prepared without the aid of proteolytic enzymes showed similar FSH stimulation of aromatase activity in the presence or absence of 10(-8) M agonist. Further, there was no evidence of degradation of the LHRH agonist when incubated with Sertoli cell cultures. From these studies, we conclude that 1) granulosa cells and Sertoli cells from immature rats differ in their responses to LHRH, and 2) the immature Sertoli cell is an unlikely target for a direct inhibiting influence of LHRH on spermatogenesis.

Animals↗