Explicating hypergonadotropism in postmenopausal women: a statistical model

2000 ◽  
Vol 278 (5) ◽  
pp. R1247-R1257 ◽  
Author(s):  
Daniel M. Keenan ◽  
Johannes D. Veldhuis
Keyword(s):  
Maximum Likelihood ◽  
Luteinizing Hormone ◽  
Slow Component ◽  
Hormone Secretion ◽  
Maximum Likelihood Estimates ◽  
Elimination Kinetics ◽  
Serum Lh ◽  
Constitutive Components ◽  
Lh Secretion ◽  
Secretion Rates

Neurohormone secretion is viewed here as a variable (unknown) admixture of basal and pulsatile release mechanisms, convolved with individually fitted biexponential elimination kinetics. This construct allows maximum-likelihood estimates of both (regulated and constitutive) components of hormone secretion. Thereby, we infer that a prolonged slow-component half-life of gonadotropin removal and amplified pulsatile (and total) daily luteinizing hormone (LH) secretion rates jointly explicate the postmenopausal elevation in serum LH concentrations without a necessary rise in basal LH secretion rates. This biomathematical formulation should be useful in exploring other neuroregulatory mechanisms that underlie single or dual alterations in the basal versus pulsatile modes of hormone secretion.

Effects of valproate-induced alteration of the GABAergic system on pulsatile luteinizing hormone secretion in ovariectomized women

1996 ◽  
Vol 135 (3) ◽  
pp. 293-298 ◽  
Author(s):  
Joaquin Lado-Abeal ◽  
Jose L Liz ◽  
Carlos Rey ◽  
Manuel Febrero ◽  
Jose Cabezas-Cerrato
Keyword(s):  
Luteinizing Hormone ◽  
Sodium Valproate ◽  
Pulse Generator ◽  
Hormone Secretion ◽  
Gabaergic System ◽  
Luteinizing Hormone Secretion ◽  
Serum Lh ◽  
Nutrition Service ◽  
Significant Difference ◽  
Lh Secretion

Lado-Abeal J, Liz JL, Rey C, Febrero M, Cabezas-Cerrato J. Effects of valproate-induced alteration of the GABAergic system on pulsatile luteinizing hormone secretion in ovariectomized women. Eur J Endocrinol 1996;135:293–8. ISSN 0804–4643 It is well established that valproate increases hypothalamic concentrations of γ-aminobutyric acid (GABA). Although little research has been done on the role of GABA in the control of pulsatile luteinizing hormone (LH) secretion in humans, our group recently found that administration of valproate had no significant effect on pulsatile LH secretion in late follicular and mid-late luteal phase normal women. However, the results of several studies of rats suggest that GABAergic regulation of LH secretion may depend on steroid levels. The objective of this work was to determine whether regular administration of sodium valproate inhibits pulsatile LH secretion in ovariectomized women. Twelve women who had undergone ovariectomy for causes other than malignant tumors were each studied in two 8 h sessions, in each of which blood samples were taken every 5 min. The first session was the control; for the second, 400 mg of sodium valproate was administered every 8 h during the seven preceding days and at 08.00 h and 14.00 h on the day of the study session. Serum valproate was determined by repolarization fluorescence spectrophotometry, and LH, estradiol and progesterone by radioimmunoassay. The serum LH series were subjected to a deconvolution procedure to reconstruct the pattern of pituitary LH secretion. Luteinizing hormone pulses were identified by the authors' nonparametric method. Control and post-valproate results were compared with regard to number of pulses, pulse duration, the quantity of LH secreted in each pulse, interpulse interval and mean serum LH level. There was no statistically significant difference between control and post-valproate results for any of the variables considered. It is concluded that sustained serum valproate levels do not alter pulsatile secretion of LH in ovariectomized women. This implies that, in humans, GABA is probably not a decisive factor in the regulation of the GnRH pulse generator. J Cabezas-Cerrato, Endocrinology and Nutrition Service, General Hospital of Galicia, c/Galeras s/n 15705, Santiago de Compostela, La Coruña, Spain

Androgenic and oestrogenic steroid participation in feedback control of luteinizing hormone secretion in male sheep

1983 ◽  
Vol 102 (4) ◽  
pp. 499-504 ◽  
Author(s):  
M. J. D'Occhio ◽  
B. D. Schanbacher ◽  
J. E. Kinder
Keyword(s):  
Luteinizing Hormone ◽  
Pulse Generator ◽  
Hormone Secretion ◽  
Pulse Interval ◽  
Serum Concentrations ◽  
Luteinizing Hormone Secretion ◽  
Lh Release ◽  
Lh Secretion ◽  
Additional Feedback ◽  
Male Sheep

Abstract. The acute castrate ram (wether) was used as an experimental model to investigate the site(s) of feedback on luteinizing hormone (LH) by testosterone, dihydrotestosterone and oestradiol. At the time of castration, wethers were implanted subdermally with Silastic capsules containing either crystalline testosterone (three 30 cm capsules), dihydrotestosterone (five 30 cm capsules) or oestradiol (one 6.5 cm capsule). Blood samples were taken at 10 min intervals for 6 h 2 weeks after implantation to determine serum steroid concentrations and to characterize the patterns of LH secretion. Pituitary LH response to exogenous LRH (5 ng/kg body weight) were also determined at the same time. The steroid implants produced serum concentrations of the respective hormones which were either one-third (testosterone) or two-to-four times (dihydrotestosterone, oestradiol) the levels measured in rams at the time of castration. Non-implanted wethers showed rhythmic pulses of LH (pulse interval 40–60 min) and had elevated LH levels (16.1 ± 1.6 ng/ml; mean ± se) 2 weeks after castration. All three steroids suppressed pulsatile LH release and reduced mean LH levels (to below 3 ng/ml) and pituitary LH responses to LRH. Inhibition of pulsatile LH secretion by all three steroids indicated that testosterone as well as its androgenic and oestrogenic metabolites can inhibit the LRH pulse generator in the hypothalamus. Additional feedback on the pituitary was indicated by the dampened LH responses to exogenous LRH.

scholarly journals Beta-endorphin/beta-lipotropin release and gonadotropin secretion after acute exercise in normal males

1986 ◽  
Vol 61 (6) ◽  
pp. 2045-2049 ◽  
Author(s):  
A. N. Elias ◽  
K. Iyer ◽  
M. R. Pandian ◽  
P. Weathersbee ◽  
S. Stone ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Acute Exercise ◽  
Suppressive Effect ◽  
Normal Male ◽  
Base Line ◽  
Gonadotropin Secretion ◽  
Beta Endorphin ◽  
Serum Lh ◽  
Normal Males ◽  
Lh Secretion

The plasma beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) response to acute exercise and the relationship of these opioid peptides to basal and luteinizing hormone-releasing hormone (LRH)-stimulated luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion was studied in eight normal male volunteers. Acute exercise resulted in a rise in plasma beta-LPH levels that returned to base line when measured 60 min after exercise. Plasma beta-EP levels did not demonstrate any rise when measured immediately after 20 min of exercise or at 60 min after exercise. Serum LH concentrations in individual volunteers declined to nadir values 60–180 min after exercise after which they showed a rebound to levels higher than the preexercise values in three of five volunteers in whom nadir LH levels were attained before the final (180 min) measurement. Serum FSH concentrations were unaltered by exercise. Acute exercise similarly did not alter the LH/FSH response to exogenous LRH stimulation. Pretreatment of the volunteers with the narcotic antagonist, naloxone, failed to alter the postexercise or LRH-stimulated LH and FSH release. The data suggest that beta-EP does not exert a suppressive effect on LH secretion after acute exercise in normal human males. Whether the suppression of LH secretion after acute exercise in unconditioned males is due to factor(s) cosecreted with beta-LPH, an increase in brain beta-EP or to alternate mechanisms such as alteration in central dopaminergic or GABAergic tone remains to be established.

scholarly journals Induction of final oocyte maturation in Cyprinidae fish by hypothalamic factors: a review

2009 ◽  
Vol 54 (No. 3) ◽  
pp. 97-110 ◽  
Author(s):  
P. Podhorec ◽  
J. Kouril
Keyword(s):  
Luteinizing Hormone ◽  
Oocyte Maturation ◽  
Hormone Secretion ◽  
Inhibitory Effect ◽  
Gonadotropin Releasing Hormone ◽  
Luteinizing Hormone Secretion ◽  
Releasing Hormone ◽  
Final Oocyte Maturation ◽  
In Captivity ◽  
Lh Secretion

Gonadotropin-releasing hormone in Cyprinidae as in other Vertebrates functions as a brain signal which stimulates the secretion of luteinizing hormone from the pituitary gland. Two forms of gonadotropin-releasing hormone have been identified in cyprinids, chicken gonadotropin-releasing hormone II and salmon gonadotropin-releasing hormone. Hypohysiotropic functions are fulfilled mainly by salmon gonadotropin-releasing hormone. The only known factor having an inhibitory effect on LH secretion in the family Cyprinidae is dopamine. Most cyprinids reared under controlled conditions exhibit signs of reproductive dysfunction, which is manifested in the failure to undergo final oocyte maturation and ovulation. In captivity a disruption of endogenous gonadotropin-releasing hormone stimulation occurs and sequentially that of luteinizing hormone, which is indispensible for the final phases of gametogenesis. In addition to methods based on the application of exogenous gonadotropins, the usage of a method functioning on the basis of hypothalamic control of final oocyte maturation and ovulation has become popular recently. The replacement of natural gonadotropin-releasing hormones with chemically synthesized gonadotropin-releasing hormone analogues characterized by amino acid substitutions at positions sensitive to enzymatic degradation has resulted in a centuple increase in the effectiveness of luteinizing hormone secretion induction. Combining gonadotropin-releasing hormone analogues with Dopamine inhibitory factors have made it possible to develop an extremely effective agent, which is necessary for the successful artificial reproduction of cyprinids.

scholarly journals Neural Determinants of Pulsatile Luteinizing Hormone Secretion in Male Mice

Endocrinology ◽  
2020 ◽  
Vol 161 (2) ◽  
Author(s):  
Su Young Han ◽  
Isaiah Cheong ◽  
Tim McLennan ◽  
Allan E Herbison
Keyword(s):  
Luteinizing Hormone ◽  
High Frequency ◽  
Pulse Generator ◽  
Hormone Secretion ◽  
Pulse Frequency ◽  
Male Mice ◽  
Intact Male ◽  
Luteinizing Hormone Secretion ◽  
Pulse Profile ◽  
Lh Secretion

Abstract The gonadotrophin-releasing hormone (GnRH) pulse generator drives pulsatile luteinizing hormone (LH) secretion essential for fertility. However, the constraints within which the pulse generator operates to drive efficient LH pulsatility remain unclear. We used optogenetic activation of the arcuate nucleus kisspeptin neurons, recently identified as the GnRH pulse generator, to assess the efficiency of different pulse generator frequencies in driving pulsatile LH secretion in intact freely behaving male mice. Activating the pulse generator at 45-minute intervals generated LH pulses similar to those observed in intact male mice while 9-minute interval stimulation generated LH profiles indistinguishable from gonadectomized (GDX) male mice. However, more frequent activation of the pulse generator resulted in disordered LH secretion. Optogenetic experiments directly activating the distal projections of the GnRH neuron gave the exact same results, indicating the pituitary to be the locus of the high frequency decoding. To evaluate the state-dependent behavior of the pulse generator, the effects of high-frequency activation of the arcuate kisspeptin neurons were compared in GDX and intact mice. The same stimulus resulted in an overall inhibition of LH release in GDX mice but stimulation in intact males. These studies demonstrate that the GnRH pulse generator is the primary determinant of LH pulse profile and that a nonlinear relationship exists between pulse generator frequency and LH pulse frequency. This may underlie the ability of stimulatory inputs to the pulse generator to have opposite effects on LH secretion in intact and GDX animals.

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.

scholarly journals Galanin Enhancement of Gonadotropin-Releasing Hormone-Stimulated Luteinizing Hormone Secretion in Female Rats Is Estrogen Dependent

Endocrinology ◽  
2003 ◽  
Vol 144 (2) ◽  
pp. 484-490 ◽  
Author(s):  
Cynthia L. Splett ◽  
Joseph R. Scheffen ◽  
Joshua A. Desotelle ◽  
Vicky Plamann ◽  
Angela C. Bauer-Dantoin
Keyword(s):  
Luteinizing Hormone ◽  
Hormone Secretion ◽  
Gonadotropin Releasing Hormone ◽  
Gonadal Steroids ◽  
Female Rats ◽  
Luteinizing Hormone Secretion ◽  
Ovx Rats ◽  
Lh Secretion ◽  
Lines Of Evidence

The hypothalamic peptide GnRH is the primary neuroendocrine signal regulating pituitary LH in females. The neuropeptide galanin is cosecreted with GnRH from hypothalamic neurons, and in vitro studies have demonstrated that galanin can act at the level of the pituitary to directly stimulate LH secretion and also augment GnRH-stimulated LH secretion. Several lines of evidence have suggested that the hypophysiotropic effects of galanin are important for the generation of preovulatory LH surges. To determine whether the pituitary actions of galanin are enhanced by the preovulatory steroidal milieu, LH responses to galanin administration (with or without GnRH) were examined in: 1) ovariectomized (OVX); 2) OVX, estrogen (E)-primed; and 3) OVX, E- and progesterone-treated female rats. Results from the study indicate that galanin enhances GnRH-stimulated LH secretion only in the presence of E (in OVX, E-primed, or E- and progesterone-treated rats). Galanin alone does not directly stimulate LH secretion under any of the steroid conditions examined. In the absence of gonadal steroids (OVX rats), galanin inhibits GnRH-stimulated LH secretion. These findings suggest that the primary pituitary effect of galanin is to modulate GnRH-stimulated LH secretion, and that the potentiating effects of galanin occur only in the presence of E.

EFFECT OF SYNTHETIC THYROTROPHIN RELEASING FACTOR ON PROLACTIN AND LUTEINIZING HORMONE SECRETION IN MALE AND FEMALE RATS DURING VARIOUS REPRODUCTIVE STATES

1975 ◽  
Vol 67 (3) ◽  
pp. 425-430 ◽  
Author(s):  
R. P. DEIS ◽  
NIA ALONSO
Keyword(s):  
Hormone Secretion ◽  
Female Rats ◽  
Male Rats ◽  
Serum Prolactin ◽  
Serum Prolactin Level ◽  
Luteinizing Hormone Secretion ◽  
Male And Female Rats ◽  
Serum Lh ◽  
The Mean ◽  
Lh Secretion

SUMMARY The effect of synthetic thyrotrophin releasing factor (TRF) on serum prolactin and LH concentrations was determined by radioimmunoassay in male, cyclic and pseudopregnant female rats. A solution of TRF (0·1, 0·25, 0·5 and 1 μg/rat) was injected i.v. at 17.00 h into rats pretreated with sodium pentobarbitone at 13.00 h. A group of male rats was also treated with TRF at 11.00 h after pretreatment with sodium pentobarbitone at 07.00 h. Fifteen minutes after TRF administration, blood samples were obtained by heart puncture. Doses of 0·25, 0·5 and 1 μg TRF significantly increased the serum prolactin concentration in pro-oestrous rats. The mean serum prolactin level after the injection of 0·5 and 1 μg into oestrous rats and 0·5 μg TRF into dioestrous day 2 rats, was significantly greater than the control values. Injection of TRF on day 1 of dioestrus had no effect. Serum LH concentration was not significantly modified by the various doses of TRF administered. On day 3 of pseudopregnancy a significant increase of serum prolactin values was obtained with 0·5 and 1 μg TRF. On day 7 of pseudopregnancy a dose of 0·5 μg produced the same effect, but on day 10 of pseudopregnancy only 1 μg TRF significantly increased serum prolactin levels when compared with the control rats. In male rats serum prolactin concentration was significantly greater than the control values after TRF treatment either in the morning or the afternoon. The response was similar to that obtained in pro-oestrous rats. The results suggest that the ability of synthetic TRF to stimulate prolactin release exists in both female and male rats and that TRF does not affect LH secretion.

FACTORS INFLUENCING THE SECRETION OF LUTEINIZING HORMONE AND OVULATION IN RESPONSE TO ELECTROCHEMICAL STIMULATION OF THE PREOPTIC AREA IN RATS

1973 ◽  
Vol 58 (2) ◽  
pp. 163-176 ◽  
Author(s):  
M. E. VELASCO ◽  
I. ROTHCHILD
Keyword(s):  
Luteinizing Hormone ◽  
Preoptic Area ◽  
Threshold Level ◽  
Peak Serum ◽  
Ovariectomized Rats ◽  
Factors Affecting ◽  
Serum Lh ◽  
The Mean ◽  
Lh Secretion ◽  
Stimulation Of

SUMMARY Factors affecting luteinizing hormone (LH) secretion in response to stimulation of the preoptic area (POA) of the forebrain in rats were explored by determining serum LH levels after electrochemical stimulation of the POA. In rats made anovulatory by exposure to constant light (CLA rats), peak concentrations of LH in serum were found 2 h after stimulation with 5–15 mC, and 1 h after stimulation with 0·5–1 mC. The peak levels increased with increasing doses between 0·5 and 15 mC. The incidence of rats ovulating and the mean number of ovulations/rat were roughly proportional to the stimulating dose, but a plateau was reached between 5 and 10 mC. A threshold level of serum LH seemed to be necessary for ovulation, and the incidence of ovulations of six ova or more/rat increased with the increase in peak serum LH level. Preoptic-roof section, which cuts dorsal afferents to the POA, enhanced the increase in serum LH in response to POA stimulation in CLA rats, while sodium pentobarbitone anaesthesia decreased the response. In both cases, the incidence of ovulation and the number of ovulations/rat were not different from values found in POA-stimulated control CLA rats showing the same peak serum LH level. In normal cyclic rats the response of serum LH to stimulation was much greater on the morning of pro-oestrus than on that of oestrus; at prooestrus a second rise occurred between 17.00 and 19.00 h. Three days after ovariectomy the basal level of LH increased; these ovariectomized rats showed a small increase in response to a dose of 5 mC. Treatment with 20 μg oestradiol benzoate at the time of ovariectomy, however, resulted in a lowered basal LH level, but the peak response to 5 mC was almost as great as that found in similarly stimulated intact CLA rats. In intact males and in neonatally androgen-treated females the peak levels of serum LH in response to doses of 5 or 15 mC were equivalent to those in CLA females in response to doses of only 1–5 mC.

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