scholarly journals Pulsatile gonadotropin-releasing hormone release from hypothalamic explants of male marmoset monkeys compared with male rats

2010 ◽  
Vol 298 (1) ◽  
pp. R70-R78 ◽  
Author(s):  
Michael J. Woller ◽  
Pam L. Tannenbaum ◽  
Nancy J. Schultz-Darken ◽  
Bruce D. Eshelman ◽  
David H. Abbott
Keyword(s):  
Species Difference ◽  
Pulse Amplitude ◽  
Gonadotropin Releasing Hormone ◽  
Male Rats ◽  
Male Rat ◽  
Releasing Hormone ◽  
Gnrh Release ◽  
Marmoset Monkeys ◽  
Release Profiles

The present study was conducted to quantify in vitro gonadotropin-releasing hormone (GnRH) release parameters in the male marmoset. We established primary cultures of marmoset hypothalamic tissues for ∼2 days (marmosets) to assess GnRH release profiles in vitro in hypothalamic explants from testis-intact and gonadectomized males. Pulsatile GnRH release profiles were readily demonstrated from in vitro hypothalamic explants isolated from adult male marmoset monkeys. Gonadectomy of male marmosets resulted in elevated mean GnRH and pulse amplitude from hypothalamic explants on the 1st day of culture ( day 0). GnRH pulse amplitude increased by day 2 in ∼67% of hypothalamic explants from testis-intact marmosets, suggesting release from an endogenous regulator of GnRH. We also measured GnRH release profiles in vitro in hypothalamic explants from testis-intact and gonadectomized rats. Male rats showed no changes in any concentration or frequency release parameters for GnRH following gonadectomy or during successive days in culture. The present study represents a unique examination of GnRH release from male marmoset monkey hypothalamic tissue and compares release dynamics directly with those obtained from male rat, suggesting a species difference in feedback regulation of GnRH release.

scholarly journals Activin-A stimulates hypothalamic gonadotropin-releasing hormone release by the explanted male rat hypothalamus: interaction with inhibin and androgens

1998 ◽  
Vol 156 (2) ◽  
pp. 269-274 ◽  
Author(s):  
AE Calogero ◽  
N Burrello ◽  
AM Ossino ◽  
P Polosa ◽  
R D'Agata
Keyword(s):  
Activin A ◽  
Gonadotropin Releasing Hormone ◽  
Male Rats ◽  
Male Rat ◽  
Maximal Effect ◽  
Dependent Manner ◽  
Releasing Hormone ◽  
Gnrh Release ◽  
Release In Vitro

The presence of activins in those hypothalamic regions containing gonadotropin-releasing hormone (GnRH)-secreting neurons suggests that these peptides may regulate the reproductive function modulating not only pituitary FSH release and biosynthesis, but also hypothalamic GnRH release. The purpose of this study was to evaluate the effects of activin-A, a homodimer of inhibin beta A subunit, on hypothalamic GnRH release in vitro and, because of their well known antithetical effects, to evaluate its interaction with inhibin. In addition, since androgens modulate the release of GnRH from male rat hypothalami, we thought it of interest to study the possible interplay between these steroids and activin on GnRH release. To accomplish this, we employed a hypothalamic organ culture system which enabled us to evaluate GnRH release from individually incubated hemi-hypothalami explanted from male rats. Activin-A stimulated GnRH release in a biphasic manner. The maximal effect was reached at a concentration of 10 ng/ml which increased GnRH output by about 75%. Inhibin abolished the stimulatory effect of a maximally effective concentration of activin-A in a dose-dependent manner, whereas alone it had no effect on GnRH output. As previously shown, testosterone (1 nmol/l) and dihydrotestosterone (DHT, 0.1 nmol/l) suppressed basal GnRH release, but only testosterone was able to inhibit the release of GnRH stimulated by activin-A. Since DHT is a non-aromatizable androgen, we evaluated whether the inhibitory effect of testosterone was due to its in vitro conversion into 17 beta-estradiol. The addition of 4-hydroxyandrostenedione, a steroidal aromatase inhibitor, did not influence the suppressive effect of testosterone on GnRH release stimulated by activin-A. In conclusion, activin-A stimulated hypothalamic GnRH release in vitro and this effect was abolished by inhibin and was blunted by testosterone. These findings suggest that activins may participate in the regulation of the hypothalamic-pituitary-gonadal axis by modulating GnRH release. The ability of testosterone to suppress the release of GnRH stimulated by activin-A indicates that this steroid has a potent negative feedback influence on GnRH release.

Estrogen stimulates gonadotropin-releasing hormone release from rat hypothalamus independently through catecholamine and histamine in vitro

1989 ◽  
Vol 120 (5) ◽  
pp. 644-648 ◽  
Author(s):  
Shirou Ohtsuka ◽  
Takamichi Nishizaki ◽  
Keiichi Tasaka ◽  
Akira Miyake ◽  
Osamu Tanizawa ◽  
...  
Keyword(s):  
Bovine Serum Albumin ◽  
Gonadotropin Releasing Hormone ◽  
Female Rats ◽  
Hormone Release ◽  
Mediobasal Hypothalamus ◽  
Releasing Hormone ◽  
Gnrh Release ◽  
Perifusion System ◽  
Made In

Abstract. Estradiol is known to stimulate gonadotropin-releasing hormone release from the rat mediobasal hypothalamus. Studies were made in an in vitro perifusion system on whether catecholamine and/or histamine was involved in estradiol-induced GnRH release. Normal cycling female rats were decapitated in diestrus II and their medio-basal hypothalami were combined and, perifused with Earl's balanced salt solution containing 0.01% bovine serum albumin bubbled with 95% O2 and 5% CO2. The levels of norepinephrine, dopamine, and histamine and of GnRH in the effluent were measured by HPLC and radioimmunoassay, respectively. Administration of 10−6 mol/l estradiol resulted in releases of norepinephrine, dopamine, histamine and GnRH at levels of 98, 70, 91 and 288%, respectively, of initial values. Administration of 10−6 mol/l norepinephrine or dopamine resulted in no increase in histamine release, and administration of 10−6 mol/l histamine did not increase release of norepinephrine or dopamine. These data suggest that estradiol stimulates the releases of GnRH, catecholamine and histamine from the rat medio-basal hypothalamus, and that it increases GnRH release independently through catecholamine and histamine. As we found previously that norepinephrine or histamine stimulates GnRH release from the mediobasal hypothalamus, we conclude that estradiol stimulates releases of norepinephrine and histamine, resulting in GnRH release from the medio-basal hypothalamus.

Ageing does not influence the ultrashort feedback control of GnRH secretion in vitro

1990 ◽  
Vol 122 (3) ◽  
pp. 329-335 ◽  
Author(s):  
Elio Messi ◽  
Mariarosa Zanisi ◽  
Luciano Martini
Keyword(s):  
Feedback Control ◽  
Experimental Period ◽  
Feedback Mechanism ◽  
Male Rats ◽  
Male Rat ◽  
Gnrh Analogue ◽  
Feedback Systems ◽  
Gnrh Secretion ◽  
Gnrh Release

Abstract. Evidence indicates that long and short feedback systems are altered in the aged male rat. Data also indicate the existence of an ultrashort feedback mechanism controlling GnRH secretion. The present experiments were performed to test whether the ultrashort feedback control of GnRH is operating also in old male rats. Mediobasal hypothalami of 18-month-old male rats were perifused in vitro either in the presence or in the absence of a GnRH agonistic analogue (Buserelin: [D-Ser(TBU)6, Des-Gly10]GnRH ethylamide) and stimulated with 5-min pulses of K+ (for a total of six pulses) in order to test their ability to release GnRH. The hypothalamic fragment was exposed to the GnRH analogue either for a part of the experimental period (at the beginning or at the end) or for the whole duration of the perifusion. In both cases, the presence of the analogue diminished or totally abolished the responses to K+ stimulation. This is in line with the results obtained in young animals. The data suggest that the ultrashort feedback mechanism controlling GnRH release is normally functioning also in aged male rats despite the fact that other types of feedback mechanisms (long and short loop) are substantially altered.

scholarly journals Pyroglutamylated RFamide Peptide 43 Stimulates the Hypothalamic-Pituitary-Gonadal Axis via Gonadotropin-Releasing Hormone in Rats

Endocrinology ◽  
2008 ◽  
Vol 149 (9) ◽  
pp. 4747-4754 ◽  
Author(s):  
Sejal R. Patel ◽  
Kevin G. Murphy ◽  
Emily L. Thompson ◽  
Michael Patterson ◽  
Annette E. Curtis ◽  
...  
Keyword(s):  
Food Intake ◽  
Intraperitoneal Administration ◽  
Gonadotropin Releasing Hormone ◽  
Male Rats ◽  
Sex Steroid ◽  
The Novel ◽  
Gnrh Release ◽  
Ad Libitum ◽  
Influence Behavior

Although it is established that other members of the RFamide family stimulate the hypothalamic-pituitary-gonadal axis, the influence of the novel pyroglutamylated RFamide peptide 43 (QRFP43) is not known. We show intracerebroventricular (icv) administration of QRFP43 (2 nmol) to male rats increased plasma LH and FSH levels at 40 min after injection. icv administration of 3 nmol QRFP43 did not affect food intake in ad-libitum-fed male rats. The icv administration of 2 nmol QRFP43 did not significantly influence behavior in male rats. Intraperitoneal administration of doses up to 1200 nmol/kg QRFP43 in male rats did not significantly influence circulating gonadotropin or sex steroid levels. In vitro, QRFP43 stimulated GnRH release from hypothalamic explants from male rats and from GT1-7 cells. Pretreatment with a GnRH receptor antagonist, cetrorelix, blocked the increase in plasma LH levels after icv administration of QRFP43 (2 nmol). These results suggest that icv QRFP43 activates the hypothalamic-pituitary-gonadal axis via GnRH.

Testosterone regulates the secretion of thyrotrophin-releasing hormone (TRH) and TRH precursor in the rat hypothalamic-pituitary axis

1990 ◽  
Vol 125 (2) ◽  
pp. 263-270 ◽  
Author(s):  
A. E. Pekary ◽  
M. Knoble ◽  
N. H. Garcia ◽  
S. Bhasin ◽  
J. M. Hershman
Keyword(s):  
In Vitro Release ◽  
Serum Levels ◽  
Male Rats ◽  
Testosterone Replacement ◽  
Male Rat ◽  
Posterior Pituitary ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Vitro Release

ABSTRACT Orchidectomy has been reported to decrease concentrations of thyrotrophin (TSH) in the circulation of male rats without affecting serum levels of thyroid hormones. To understand the mechanism underlying this observation, we have measured the effect of gonadal status on the in-vitro release of TSH-releasing hormone (TRH) by male rat hypothalamic fragments. Because hormone release rates can be affected by changes in the post-translational processing of the hormonal precursors, we have also studied the corresponding changes in the concentrations of TRH and TRH-Gly, a TRH precursor peptide in hypothalamus and pituitary, by radioimmunoassay. We observed a significant decline in the in-vitro release of TRH from incubated hypothalami 1 week after castration, which was quantitatively reversed by testosterone replacement. Concentrations of TRH and TRH-Gly in the posterior pituitary, on the other hand, which derive from neurones of hypothalamic origin, increased significantly with castration and were returned to the normal range by testosterone replacement. We conclude that the primary effect of testosterone is the stimulation of hypothalamic TRH release, resulting in the depletion of TRH and TRH precursors from TRH-containing neurones which project into the median eminence and posterior pituitary. Journal of Endocrinology (1990) 125, 263–270

The neuroactive steroid allopregnanolone suppresses hypothalamic gonadotropin-releasing hormone release through a mechanism mediated by the gamma-aminobutyric acidA receptor

1998 ◽  
Vol 158 (1) ◽  
pp. 121-125 ◽  
Author(s):  
AE Calogero ◽  
MA Palumbo ◽  
AM Bosboom ◽  
N Burrello ◽  
E Ferrara ◽  
...  
Keyword(s):  
Gabaa Receptor ◽  
Gonadotropin Releasing Hormone ◽  
Neuroactive Steroids ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Hpg Axis ◽  
Releasing Hormone ◽  
Brain Functions ◽  
Gnrh Release

The central nervous system (CNS) is able to synthesize and/or metabolize steroid hormones. These neuroactive steroids are capable of modulating several brain functions and, among these, they seem to regulate the hypothalamic-pituitary-gonadal (HPG) axis. Indeed, recent observations have shown that 5 alpha-pregnane-3 alpha-ol-20-one (allopregnanolone), one of the most abundant naturally occurring neuroactive steroids, suppresses ovulation and sexual behaviour when administered within the CNS. The present study was undertaken to evaluate the effects of allopregnanolone and its inactive stereoisomer, 5 alpha-pregnane-3 beta-ol-20-one, upon the release of gonadotropin-releasing hormone (GnRH) from individually-incubated hemihypothalami. Allopregnanolone suppressed GnRH release in a concentration-dependent manner with maximal activity in the nanomolar range, a range at which this neurosteroid is capable of playing a biological action. The specificity of allopregnanolone suppression of GnRH release was provided by the lack of effect of its known inactive stereoisomer. To evaluate the involvement of gamma-aminobutyric acidA (GABAA) receptor, we examined the effects of two neurosteroids with GABA-antagonistic properties, pregnanolone sulfate (PREG-S) and dehydroepiandrosterone sulfate (DHEAS), and of bicuculline, a selective antagonist of the GABA binding site on the GABAA receptor, on allopregnanolone (10 nM)-suppressed GnRH release. Both PREG-S and bicuculline overcame the inhibitory effects of allopregnanolone on GnRH release, whereas DHEAS did not. To substantiate the involvement of the GABAA receptor further, we tested the effects of muscimol, a selective agonist for this receptor, which suppressed GnRH release. In conclusion, allopregnanolone suppressed hypothalamic GnRH release in vitro and this effect appeared to be mediated by an interaction with the GABAA receptor. We speculate that the inhibitory effect of allopregnanolone on the HPG axis may also be caused by its ability to suppress hypothalamic GnRH release.

Prolactin stimulates [ 3H]dopamine release from dispersed rat tubero-infundibular dopaminergic neurons and dopamine decreases gonadotropin-releasing hormone release induced by calcium ionophore

1993 ◽  
Vol 129 (6) ◽  
pp. 548-553 ◽  
Author(s):  
Koji Koike ◽  
Kozo Kadowaki ◽  
Kenji Hirota ◽  
Masahide Ohmichi ◽  
Hiromasa Ikegami ◽  
...  
Keyword(s):  
Dopaminergic Neurons ◽  
Dopamine Release ◽  
Primary Cultures ◽  
Calcium Ionophore ◽  
Adenosine Monophosphate ◽  
Inhibitory Effect ◽  
Gonadotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Gnrh Release

In order to investigate the involvement of prolactin-dopamine and dopamine-gonadotropin interactions in the hypothalamo-pituitary axis of hyperprolactinemia, in vitro studies were performed using primary cultures of dispersed rat hypothalamic heterogeneous cells containing tubero-infundibular dopaminergic neurons or gonadotropin-releasing hormone (GnRH) neurons. We observed that prolactin caused dose-dependent stimulation of [3H]dopamine release after a 16-h incubation. Staurosporin (10 nmol/l), an inhibitor of protein kinase C, significantly reduced the [3H]dopamine release induced by prolactin (1 mg/l). Incubation of tubero-infundibular dopaminergic neurons with prolactin (1 mg/l) had no effect on intracellular cyclic adenosine monophosphate accumulation. Dopamine (1 μmol/l) significantly (p < 0.01) reduced the release of GnRH induced by 50 μmol/l calcium ionophore from dispersed hypothalamic cells from the preoptic area, while prolactin had no effect on GnRH release. These data support the hypothesis that the antigonadotropic effect of prolactin on the hypothalamus is mediated by an inhibitory effect of dopamine on GnRH release.

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