scholarly journals No Evidence That RFamide-Related Peptide 3 Directly Modulates LH Secretion in the Ewe

Endocrinology ◽  
2016 ◽  
Vol 157 (4) ◽  
pp. 1566-1575 ◽  
Author(s):  
C. Decourt ◽  
K. Anger ◽  
V. Robert ◽  
D. Lomet ◽  
J. Bartzen-Sprauer ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Estradiol Benzoate ◽  
Inhibitory Effect ◽  
Minor Role ◽  
Gonadotropin Secretion ◽  
Related Peptide ◽  
Lh Pulsatility ◽  
Lh Release ◽  
A Minor ◽  
Lh Secretion

Abstract The neuropeptide RFamide-related peptide 3 (RFRP-3) has been implicated in the control of gonadotropin secretion in both birds and mammals. However, in mammals, depending on species, sex and photoperiod, inhibitory, excitatory, or no effect of RFRP-3 on the plasma concentration of LH has been reported. In the ewe, treatment with RFRP-3 either reduced LH concentration or had no effect, and treatment with an RFRP-3 receptor antagonist (ie, RF9) resulted in increased concentration of plasma LH. To clarify these conflicting results in the present study, a set of experiments was performed in ewes. Multiple iv injections of RFRP-3 (6 × 50 μg) in ovariectomized ewes had no effect on plasma LH pulsatility. In intact ewes a bolus injection (500 μg) or an injection (250, 500, or 1000 μg) followed by a 4-hour perfusion (250, 500, or 1000 μg · h−1) of RFRP-3 had no effect on the LH pulse induced by kisspeptin (6.5 μg). In ovariectomized, estrogen-replaced ewes, the LH surge induced by estradiol benzoate was not modified by a 24-hour perfusion of RFRP-3 (500 μg h−1). Finally, although treatment with RF9 induced a robust release of LH, treatment with a more selective RFRP-3 receptor antagonist, GJ14, resulted in no evident increase of LH. In contrast to the inhibitory effect previously suggested, our data are more consistent with the concept that RFRP-3 has no direct effect on LH secretion in ewes and that RF9 effect on LH release is likely not RFRP-3 receptor mediated. Hence, RFRP-3 probably has a minor role on the control of LH secretion in the ewe.

Plasma β-endorphin and LH during prolonged hypoglycaemia in ewes

1993 ◽  
Vol 1993 ◽  
pp. 93-93 ◽  
Author(s):  
A.M.X. Eloy ◽  
R.G. Rodway
Keyword(s):  
Plasma Concentrations ◽  
Reproductive Function ◽  
Opioid Peptide ◽  
Inhibitory Effect ◽  
Elevated Plasma ◽  
Lh Release ◽  
Lh Secretion

Normal reproductive function in female animals can be drastically impaired by a variety of stressful stimuli. For example, undernutrition and hypoglycaemia in sheep have been shown to suppress pulsatile LH secretion and to reduce the number of ewes showing pre-ovulatory LH peaks (Crump and Rodway 1986, Clarke et al. 1990). Similar stresses are also known to cause release of the opioid peptide β-endorphin into the circulation. Opioids are well-known to have a central inhibitory effect on LH release, although whether the elevated plasma concentrations of these peptides have any effect on LH secretion is unclear. The present study investigated the affect of insulin-induced hypoglycaemia on plasma concentrations of β-endorphin and LH.

scholarly journals Kallmann’s Syndrome: A Comparison of the Reproductive Phenotypes in Men Carrying KAL1 and FGFR1/KAL2 Mutations

2008 ◽  
Vol 93 (3) ◽  
pp. 758-763 ◽  
Author(s):  
Sylvie Salenave ◽  
Philippe Chanson ◽  
Hélène Bry ◽  
Michel Pugeat ◽  
Sylvie Cabrol ◽  
...  
Keyword(s):  
Plasma Level ◽  
Pubertal Development ◽  
Hypogonadotropic Hypogonadism ◽  
Gonadotropin Secretion ◽  
Lh Pulsatility ◽  
Kallmann's Syndrome ◽  
Severe Impairment ◽  
Basal Plasma ◽  
Kallmann’S Syndrome ◽  
Lh Secretion

Abstract Context: Kallmann’s syndrome (KS) is a genetically heterogeneous disorder consisting of congenital hypogonadotropic hypogonadism (CHH) with anosmia or hyposmia. Objective: Our objective was to compare the reproductive phenotypes of men harboring KAL1 and FGFR1/KAL2 mutations. Design and Patients: We studied the endocrine features reflecting gonadotropic-testicular axis function in 39 men; 21 had mutations in KAL1 and 18 in FGFR1/KAL2, but none had additional mutations in PROK-2 or PROKR-2 genes. Results: Puberty failed to occur in the patients with KAL1 mutations, all of whom had complete CHH. Three patients with FGFR1/KAL2 mutations had normal puberty, were eugonadal, and had normal testosterone and gonadotropin levels. Cryptorchidism was more frequent (14 of 21 vs. 3 of 15; P < 00.1) and testicular volume (2.4 ± 1.1 vs. 5.4 ± 2.4 ml; P < 0.001) was smaller in CHH subjects with KAL1 mutations than in subjects with FGFR1/KAL2 mutations. The mean basal plasma FSH level (0.72 ± 0.47 vs. 1.48 ± 0.62 IU/liter; P < 0.05), serum inhibin B level (19.3 ± 10.6 vs. 39.5 ± 19.3 pg/ml; P < 0.005), basal LH plasma level (0.57 ± 0.54 vs. 1.0 ± 0.6 IU/liter; P < 0.01), and GnRH-stimulated LH plasma level (1.2 ± 1.0 vs. 4.1 ± 3.5 IU/liter; P < 0.01) were significantly lower in the subjects with KAL1 mutations. LH pulsatility was studied in 13 CHH subjects with KAL1 mutations and seven subjects with FGFR1/KAL2 mutations; LH secretion was nonpulsatile in all the subjects, but mean LH levels were lower in those with KAL1 mutations. Conclusion: KAL1 mutations result in a more severe reproductive phenotype than FGFR1/KAL2 mutations. The latter are associated with a broader spectrum of pubertal development and with less severe impairment of gonadotropin secretion.

scholarly journals The Gonadotropin-Releasing Hormone Pulse Generator

Endocrinology ◽  
2018 ◽  
Vol 159 (11) ◽  
pp. 3723-3736 ◽  
Author(s):  
Allan E Herbison
Keyword(s):  
Arcuate Nucleus ◽  
Pulse Generator ◽  
Pulse Generation ◽  
Sufficient Evidence ◽  
Gnrh Neuron ◽  
Lh Pulsatility ◽  
Intrinsic Mechanism ◽  
Lh Release ◽  
Lh Secretion ◽  
Present Understanding

Abstract The pulsatile release of GnRH and LH secretion is essential for fertility in all mammals. Pulses of LH occur approximately every hour in follicular-phase females and every 2 to 3 hours in luteal-phase females and males. Many studies over the last 50 years have sought to identify the nature and mechanism of the “GnRH pulse generator” responsible for pulsatile LH release. This review examines the characteristics of pulsatile hormone release and summarizes investigations that have led to our present understanding of the GnRH pulse generator. There is presently little compelling evidence for an intrinsic mechanism of pulse generation involving interactions between GnRH neuron cell bodies. Rather, data support the presence of an extrinsic pulse generator located within the arcuate nucleus, and attention has focused on the kisspeptin neurons and their projections to GnRH neuron dendrons concentrated around the median eminence. Sufficient evidence has been gathered in rodents to conclude that a subpopulation of arcuate kisspeptin neurons is, indeed, the GnRH pulse generator. Findings in other species are generally compatible with this view and suggest that arcuate/infundibular kisspeptin neurons represent the mammalian GnRH pulse generator. With hindsight, it is likely that past arcuate nucleus multiunit activity recordings have been from kisspeptin neurons. Despite advances in identifying the cells forming the pulse generator, almost nothing is known about their mechanisms of synchronicity and the afferent hormonal and transmitter modulation required to establish the normal patterns of LH pulsatility in mammals.

Dopamine involvement in the regulation of gonadotropin secretion in coho salmon

1986 ◽  
Vol 64 (6) ◽  
pp. 1245-1248 ◽  
Author(s):  
Glen Van Der Kraak ◽  
Edward M. Donaldson ◽  
John P. Chang
Keyword(s):  
Body Weight ◽  
Coho Salmon ◽  
Effective Means ◽  
Rapid Onset ◽  
Minor Role ◽  
Gonadotropin Secretion ◽  
Luteinizing Hormone Releasing Hormone ◽  
Gonadotropin Release ◽  
A Minor ◽  
Magnitude Increase

The effects of intraperitoneal injections of [D-Ala6,Pro9-N-ethylamide]-luteinizing hormone-releasing hormone (LHRH-A) and pimozide, a dopamine receptor antagonist, on plasma gonadotropin levels and ovulation in coho salmon were investigated. Both LHRH-A (0.02 mg/kg body weight) and pimozide (10 mg/kg body weight) stimulate gonadotropin secretion, with LHRH-A causing a more rapid onset of gonadotropin release and a higher magnitude increase in plasma gonadotropin levels than pimozide. Pimozide caused a marked potentiation of the gonadotropin release response to LHRH-A. Injections of LHRH-A alone and in combination with pimozide were effective means of inducing ovulation, whereas pimozide alone was ineffective. These data support the concept that dopamine participates in the regulation of gonadotropin secretion in teleosts and suggest that dopamine has a minor role in the regulation of ovulatory gonadotropin changes in coho salmon compared with cyprinids.

Evidence for an increased opioid inhibition of LH secretion in hyperprolactinaemic ovariectomized rats

1984 ◽  
Vol 101 (1) ◽  
pp. 57-61 ◽  
Author(s):  
D. A. Carter ◽  
J. S. Cooper ◽  
S. E. Inkster ◽  
S. A. Whitehead
Keyword(s):  
Positive Feedback ◽  
Day Treatment ◽  
Inhibitory Effect ◽  
Ovariectomized Rats ◽  
Dopamine Antagonist ◽  
Similar Treatment ◽  
Lh Surge ◽  
Lh Release ◽  
Ovine Prolactin ◽  
Lh Secretion

ABSTRACT The effects of acute and sub-chronic hyperprolactinaemia on the positive feedback action of progesterone in oestrogen-primed ovariectomized rats have been compared. A single injection of ovine prolactin administered with progesterone had no effect on the LH surge measured 5 h later although hyperprolactinaemia induced by 5-day treatment with the dopamine antagonist, domperidone, markedly attenuated the surge. Repeated injections of naloxone (5 mg/kg) during the development of the progesterone-stimulated LH surge completely reversed this inhibitory effect of hyperprolactinaemia, but had no apparent effect on the positive feedback action in control animals. In oestrogen-primed animals similar treatment with naloxone (0·4 and 5 mg/kg) stimulated LH secretion but the increase was significantly smaller than that observed after injecting progesterone. It is suggested that hyperprolactinaemia increases the inhibitory opioid modulation of LH release and that this effect is responsible for the impairment of the positive feedback action of progesterone. J. Endocr. (1984) 101, 57–61

Prolactin- and testosterone-induced inhibition of LH secretion after orchidectomy: role of catecholaminergic neurones terminating in the diagonal band of Broca, medial preoptic nucleus and median eminence

1996 ◽  
Vol 148 (2) ◽  
pp. 291-301 ◽  
Author(s):  
S-K Park ◽  
D A Strouse ◽  
M Selmanoff
Keyword(s):  
Median Eminence ◽  
Inhibitory Effect ◽  
Male Rats ◽  
Testosterone Replacement ◽  
Preoptic Nucleus ◽  
Medial Preoptic Nucleus ◽  
Diagonal Band ◽  
Lh Release ◽  
Diagonal Band Of Broca ◽  
Lh Secretion

Abstract Central catecholaminergic neurones projecting to specific hypothalamic structures are involved in stimulating and inhibiting the activity of the GnRH-containing neurosecretory neurones. Both testosterone and elevated circulating prolactin (PRL) levels inhibit postcastration LH release. Three groups of adult male rats were orchidectomized and adrenalectomized, received corticosterone replacement and were: (i) administered purified ovine PRL (oPRL; 2400 μg/s.c. injection) or (ii) its diluent, polyvinylpyrrolidone (PVP), every 12 h, or (iii) received physiological testosterone replacement for 2 days. At 0, 2 and 6 days postcastration, norepinephrine (NE), epinephrine (E) and dopamine (DA) turnover were estimated by the α-methyl-p-tyrosine method in three micro-dissected hypothalamic structures: the diagonal band of Broca at the level of the organum vasculosum of the lamina terminalis (DBB(ovlt)), the medial preoptic nucleus (MPN) and the median eminence (ME). In control (PVP-treated) rats, serum LH concentrations increased eightfold at 2 and 6 days postcastration and this rise was prevented by testosterone. oPRL treatment transiently suppressed LH secretion at 2 but not 6 days postcastration. Castration significantly decreased basal rat PRL (rPRL) levels at 2 and 6 days and testosterone administration partially prevented this effect. NE turnover in the ME and E turnover in the MPN increased markedly at 2 and 6 days postcastration, and testosterone replacement for 2 days prevented these increases. Thus, noradrenergic neurones innervating the ME and adrenergic neurones innvervating the MPN may drive postcastration LH secretion by providing stimulatory afferent input to the GnRH neurones. It was striking to observe that oPRL blocked the increases in both ME NE and MPN E turnover at 2 but not 6 days postcastration. Hence, oPRL may transiently suppress LH release by an inhibitory action on these NE and E neurones. DA turnover in the DBB(ovlt) was significantly decreased by 6 days postcastration. Testosterone-treated (2 days postcastration) and oPRL-treated (2 and 6 days postcastration) rats exhibited turnover values indistinguishable from day 0 controls. Hence, the A14 dopaminergic neurones, which synapse on GnRH neurones in the rostral preoptic area and may exert an inhibitory effect on them, are positively regulated by PRL and perhaps by testosterone as well. Autoregulatory feedback suppression of endogenous rPRL secretion by oPRL was observed both 2 and 6 days postcastration. In contrast to the A14 dopaminergic neurones, turnover in the A12 tuberoinfundibular dopaminergic (TIDA) neurones innervating the ME increased significantly by 6 days postcastration in control rats while oPRL administration further increased ME DA turnover at both 2 and 6 days. Hence, autofeedback regulation of rPRL secretion persists through at least 6 days of oPRL exposure temporally associated with markedly increased turnover in the TIDA neurones. In summary, our results support the hypothesis that the inhibitory effect of PRL on postcastration LH release is mediated by suppression of the activity of NE neurones innervating the ME and E neurones terminating in the MPN which, with time, become refractory to continued PRL exposure. Journal of Endocrinology (1996) 148, 291–301

scholarly journals RFamide-Related Peptide-3 Receptor Gene Expression in GnRH and Kisspeptin Neurons and GnRH-Dependent Mechanism of Action

Endocrinology ◽  
2012 ◽  
Vol 153 (8) ◽  
pp. 3770-3779 ◽  
Author(s):  
Mohammed Z. Rizwan ◽  
Matthew C. Poling ◽  
Maggie Corr ◽  
Pamela A. Cornes ◽  
Rachael A. Augustine ◽  
...  
Keyword(s):  
Neuronal Network ◽  
Receptor Gene ◽  
Male Rats ◽  
Gonadotropin Secretion ◽  
Female Mice ◽  
Related Peptide ◽  
Gnrh Neurons ◽  
Lh Secretion ◽  
G Protein Coupled

RFamide-related peptide-3 (RFRP-3) is known to inhibit the activity of GnRH neurons. It is not yet clear whether its G protein-coupled receptors, GPR147 and GPR74, are present on GnRH neurons or on afferent inputs of the GnRH neuronal network or whether RFRP-3 can inhibit gonadotropin secretion independently of GnRH. We tested the following: 1) whether GnRH is essential for the effects of RFRP-3 on LH secretion; 2) whether RFRP-3 neurons project to GnRH and rostral periventricular kisspeptin neurons in mice, and 3) whether Gpr147 and Gpr74 are expressed by these neurons. Intravenous treatment with the GPR147 antagonist RF9 increased plasma LH concentration in castrated male rats but was unable to do so in the presence of the GnRH antagonist cetrorelix. Dual-label immunohistochemistry revealed that approximately 26% of GnRH neurons from male and diestrous female mice were apposed by RFRP-3 fibers, and 19% of kisspeptin neurons from proestrous female mice were apposed by RFRP-3 fibers. Using immunomagnetic purification of GnRH and kisspeptin cells, single-cell nested RT-PCR, and in situ hybridization, we showed that 33% of GnRH neurons and 9–16% of rostral periventricular kisspeptin neurons expressed Gpr147, whereas Gpr74 was not expressed in either population. These data reveal that RFRP-3 can act at two levels of the GnRH neuronal network (i.e. the GnRH neurons and the rostral periventricular kisspeptin neurons) to modulate reproduction but is unable to inhibit gonadotropin secretion independently of GnRH.

scholarly journals Ovarian stimulation with FSH reduces phosphorylation of gonadotrope progesterone receptor and LH secretion in the rat

Reproduction ◽  
2009 ◽  
Vol 137 (1) ◽  
pp. 151-159 ◽  
Author(s):  
Ana Gordon ◽  
José C Garrido-Gracia ◽  
Rafaela Aguilar ◽  
Silvia Guil-Luna ◽  
Yolanda Millán ◽  
...  
Keyword(s):  
Progesterone Receptor ◽  
Ovarian Stimulation ◽  
Inhibitory Effect ◽  
Ovx Rats ◽  
Formalin Fixed Paraffin ◽  
Formalin Fixed Paraffin Embedded ◽  
Experimental Approaches ◽  
Lh Release ◽  
Lh Secretion

Administration of human FSH (hFSH) to cyclic rats during the dioestrous phase attenuates progesterone receptor (PR)-dependent events of the preovulatory LH surge in pro-oestrus. The increased bioactivity of the putative ovarian gonadotropin surge inhibiting/attenuating factor induced by hFSH treatment is not associated with a decrease in PR protein expression, and the possibility of its association at a PR posttranslational effect has been raised. The present experiments aimed to analyse PR phosphorylation status in the gonadotrope of rats with impaired LH secretion induced byin vivohFSH injection. Two experimental approaches were used. First, incubated pro-oestrous pituitaries from hFSH-injected cycling and oestrogen-treated ovariectomized (OVX) rats were used to analyze the effect of calyculin, an inhibitor of intracellular phosphatases, on PR-dependent LH release, which was measured in the incubation medium by RIA. Second, pituitaries taken from hFSH-injected intact cycling and OVX rats and later incubated with P or GNRH1 were used to assess the phosphorylation rate of gonadotrope. The latter was analysed in formalin-fixed, paraffin-embedded tissue sections by immunohistochemistry using a MAB that recognizes the phosphorylated (p) form of PR at Ser294. Calyculin reduced the ovary-mediated inhibition of hFSH in GNRH1-stimulated LH secretion. In addition, the immunohistochemical expression of pSer294 PR was significantly reduced after ovarian stimulation with hFSH in pituitaries from pro-oestrous rats incubated with P or GNRH1. Altogether, these results suggested that the ovarian-dependent inhibitory effect of FSH injection on the preovulatory LH secretion in the rat may involve an increase in dephosphorylation of PR.

L-type calcium channels in the renal microcirculatory response to endothelin

2005 ◽  
Vol 288 (4) ◽  
pp. F771-F777 ◽  
Author(s):  
David M. Pollock ◽  
John M. Jenkins ◽  
Anthony K. Cook ◽  
John D. Imig ◽  
Edward W. Inscho
Keyword(s):  
Rat Kidney ◽  
Inhibitory Effect ◽  
Minor Role ◽  
Channel Blockade ◽  
Drug Infusion ◽  
Vasoconstrictor Response ◽  
A Minor ◽  
Dose Dependent ◽  
Arteriolar Diameter

The signaling pathways of endothelin (ET)-1-mediated vasoconstriction in the renal circulation have not been elucidated but appear to be distinct between ETA and ETB receptors. The purpose of this study was to determine the role of L-type Ca2+ channels in the vasoconstrictor response to ET-1 and the ETB receptor agonist sarafotoxin 6c (S6c) in the rat kidney. Renal blood flow (RBF) was measured with an ultrasonic flow probe in anesthetized rats, and a microcatheter was inserted into the renal artery for drug infusion. All rats were given vehicle (0.9% NaCl) or three successive bolus injections (1, 10, and 100 pmol) of ET-1 or S6c at 30-min intervals ( n = 6 in each group). ET-1 and S6c produced dose-dependent decreases in RBF. The Ca2+ channel blocker nifedipine (1.5 μg) significantly attenuated the RBF response only at the highest doses of ET-1 and S6c. In the isolated blood-perfused juxtamedullary nephron preparation, Ca2+ channel blockade with diltiazem had a very small inhibitory effect on ET-1-induced decreases in afferent arteriolar diameter only at the lowest concentrations of ET-1. In vascular smooth muscle cells isolated from preglomerular vessels, ET-1 produced a typical biphasic Ca2+ response, whereas S6c had no effect on cytosolic Ca2+. Furthermore, Ca2+ channel blockade (diltiazem or Ni2+) had no effect on the peak or sustained increase in cytosolic Ca2+ produced by ET-1. These results support the hypothesis that L-type Ca2+ channels play only a minor role in the constrictor responses to ET-1 in the renal microcirculation.

scholarly journals Interactions of insulin-like growth factor-I, insulin and estradiol with GnRH-stimulated luteinizing hormone release from female rat gonadotrophs

2001 ◽  
pp. 73-79 ◽  
Author(s):  
YX Xia ◽  
JM Weiss ◽  
S Polack ◽  
K Diedrich ◽  
O Ortmann
Keyword(s):  
Pituitary Cells ◽  
Female Rat ◽  
Serum Free Medium ◽  
Free Medium ◽  
Estradiol Treatment ◽  
Gonadotropin Secretion ◽  
Serum Free ◽  
Igf I ◽  
Lh Release ◽  
Lh Secretion

BACKGROUND: It is well established that ovarian steroids modulate gonadotropin secretion from anterior pituitary cells. It has been speculated that insulin and IGF-I might influence gonadotropin secretion. OBJECTIVE: To investigate the effects of IGF-I and estradiol alone, or combinations of IGF-I with insulin and estradiol on GnRH-stimulated LH release from female rat pituitary cells in serum-supplemented and serum-free culture conditions. METHODS: Pituitary cells were incubated for 24 h or 48 h with a series of increasing concentrations of IGF-I or estradiol and stimulated with 1 nmol/l GnRH for 3 h. To determine the interaction of IGF-I and estradiol on GnRH-stimulated LH secretion, cells were exposed to increasing concentrations of IGF-I and 100 pmol/l estradiol for 24 h. We also investigated the effects of combined treatment with IGF-I and insulin on GnRH-stimulated LH secretion. RESULTS: Our findings indicate that long-term IGF-I treatment (24 h) alone has a significant augmenting effect on GnRH-stimulated LH release in serum-free medium only, with a maximum at low concentrations (10 and 100 pmol/l). Estradiol significantly increased GnRH-induced LH release in a dose-dependent manner. The extent of GnRH-stimulated LH secretion by long-term estradiol treatment (24 h) was significantly greater in serum-supplemented (+42%) medium than in serum-free medium. Estradiol facilitated IGF-I-primed LH responses to GnRH in serum-free medium. In contrast, in serum-supplemented medium, the facilitating potential of estradiol was lower. We also found that, in GnRH-stimulated cells, LH release was augmented by insulin treatment, in contrast to quiescent cells that had been pretreated with 100 pmol/l IGF-I alone and 1 nmol/l insulin alone. CONCLUSIONS: IGF-I and to a lesser extent insulin stimulate GnRH-induced LH secretion from pituitary gonadotrophs. This action is enhanced by estradiol treatment of the cells. However, the well known stimulatory action of estradiol on LH secretion is dependent on the presence of growth factors.

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