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 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.

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.

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.

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.

scholarly journals Estradiol Enables Chronic Corticosterone to Inhibit Pulsatile Luteinizing Hormone Secretion and Suppress Kiss1 Neuronal Activation in Female Mice

2019 ◽  
Vol 110 (6) ◽  
pp. 501-516 ◽  
Author(s):  
Michael J. Kreisman ◽  
Richard B. McCosh ◽  
Katherine Tian ◽  
Christopher I. Song ◽  
Kellie M. Breen
Keyword(s):  
Luteinizing Hormone ◽  
Hormone Secretion ◽  
Pulse Frequency ◽  
Dependent Manner ◽  
Neuronal Activation ◽  
Luteinizing Hormone Secretion ◽  
Female Mice ◽  
Enhanced Sensitivity ◽  
Ovarian Cyclicity ◽  
Lh Secretion

Introduction: Two common responses to stress include elevated circulating glucocorticoids and impaired luteinizing hormone (LH) secretion. We have previously shown that a chronic stress level of corticosterone can impair ovarian cyclicity in intact mice by preventing follicular-phase endocrine events. Objective: This study is aimed at investigating if corticosterone can disrupt LH pulses and whether estradiol is necessary for this inhibition. Methods: Our approach was to measure LH pulses prior to and following the administration of chronic corticosterone or cholesterol in ovariectomized (OVX) mice treated with or without estradiol, as well as assess changes in arcuate kisspeptin (Kiss1) neuronal activation, as determined by co-expression with c-Fos. Results: In OVX mice, a chronic 48 h elevation in corticosterone did not alter the pulsatile pattern of LH. In contrast, corticosterone induced a robust suppression of pulsatile LH secretion in mice treated with estradiol. This suppression represented a decrease in pulse frequency without a change in amplitude. We show that the majority of arcuate Kiss1 neurons contain glucocorticoid receptor, revealing a potential site of corticosterone action. Although arcuate Kiss1 and Tac2 gene expression did not change in response to corticosterone, arcuate Kiss1 neuronal activation was significantly reduced by chronic corticosterone, but only in mice treated with estradiol. Conclusions: Collectively, these data demonstrate that chronic corticosterone inhibits LH pulse frequency and reduces Kiss1 neuronal activation in female mice, both in an estradiol-dependent manner. Our findings support the possibility that enhanced sensitivity to glucocorticoids, due to ovarian steroid milieu, may contribute to reproductive impairment associated with stress or pathophysiologic conditions of elevated glucocorticoids.

Age-Related Changes in the Regulation of Luteinizing Hormone Secretion by Estrogen in Women

2002 ◽  
Vol 227 (7) ◽  
pp. 455-464 ◽  
Author(s):  
Susanna J. Park ◽  
Laura T. Goldsmith ◽  
Gerson Weiss
Keyword(s):  
Menstrual Cycle ◽  
Luteinizing Hormone ◽  
Hormone Secretion ◽  
Luteinizing Hormone Secretion ◽  
Estrogen Regulation ◽  
Lh Surge ◽  
Age Related ◽  
Hypothalamic Pituitary Axis ◽  
The Many ◽  
Lh Secretion

Despite the many studies that have been conducted using both primate and human models to understand the control of the menstrual cycle, there are many aspects of the hormonal dynamics of the menstrual cycle that are not understood. This Minireview summarizes the changes in estrogen regulation of luteinizing hormone (LH) secretion that occur throughout life in women from the time of maturation of the hypothalamic-pituitary axis resulting in the occurrence of the LH surge during puberty, through the reproductive years, to the changes in the regulation of the LH surge during premenopause and, subsequently, menopause.

IMPORTANCE OF THE EPISODIC NATURE OF LUTEINIZING HORMONE SECRETION FOR NORMAL DEVELOPMENT OF THE BOVINE TESTIS DURING PUBERTY: INTERFERENCE WITH OESTRADIOL-17β

1981 ◽  
Vol 88 (3) ◽  
pp. 393-400 ◽  
Author(s):  
B. D. SCHANBACHER
Keyword(s):  
Normal Development ◽  
Pubertal Development ◽  
Hormone Secretion ◽  
Serum Testosterone ◽  
Luteinizing Hormone Secretion ◽  
Testicular Growth ◽  
Serum Lh ◽  
Beef Bulls ◽  
Lh Releasing Hormone ◽  
Lh Secretion

An experiment was conducted to determine the importance of episodic LH secretion during pubertal development in beef bulls. Testicular growth, LH secretory patterns and serum testosterone concentrations were monitored in control bulls, and bulls implanted with one or two oestradiol-filled capsules from 26 to 38 weeks of age. Control but not oestradiol-treated bulls showed normal testicular growth and episodic LH secretory patterns. Serum LH and testosterone responses of 38-week-old control and oestradiol-treated bulls to an intravenous challenge of 5 μg LH releasing hormone indicated normal pituitary responsiveness, but steroidogenic responsiveness had not yet developed in oestradiol-treated bulls. Removal of the capsules at 38 weeks of age resulted in a normal episodic release pattern for LH, with concomitant growth of the underdeveloped testes up to 44 weeks of age. Serum concentrations of LH and testosterone were within the range of normal, adult values by 42 weeks of age. These results suggest that oestradiol can interfere with episodic LH secretion and normal pubertal development in beef bulls, and furthermore that episodic LH secretion is commensurate with the establishment of normal development of the bovine testis during puberty.

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