Role of Forebrain Structures in the Regulation of Gonadotropin Secretion

2015 ◽  
pp. 101-113
Author(s):  
Masazumi Kawakami ◽  
Fukuko Kimura ◽  
Nobuhide Konda
Keyword(s):  
Gonadotropin Secretion

scholarly journals Differential Control of Gonadotropin Secretion in the Human: Endocrine Role of Inhibin1

1998 ◽  
Vol 83 (6) ◽  
pp. 1835-1841 ◽  
Author(s):  
Frances J. Hayes ◽  
Janet E. Hall ◽  
Paul A. Boepple ◽  
William F. Crowley
Keyword(s):  
Gonadotropin Secretion ◽  
Differential Control

Role of Peptides in the Control of Gonadotropin Secretion

1984 ◽  
pp. 3-25 ◽  
Author(s):  
S. M. McCann ◽  
G. D. Snyder ◽  
S. R. Ojeda ◽  
M. D. Lumpkin ◽  
A. Ottlecz ◽  
...  
Keyword(s):  
Gonadotropin Secretion

scholarly journals The Role of Growth Hormone in the Control of Gonadotropin Secretion in Adult Male Rats*

Endocrinology ◽  
1998 ◽  
Vol 139 (3) ◽  
pp. 1067-1074 ◽  
Author(s):  
Varadaraj Chandrashekar ◽  
Andrzej Bartke
Keyword(s):  
Growth Hormone ◽  
Adult Male ◽  
Male Rats ◽  
Gonadotropin Secretion

scholarly journals Reproductive capacity in iron overloaded women with thalassemia major

Blood ◽  
2011 ◽  
Vol 118 (10) ◽  
pp. 2878-2881 ◽  
Author(s):  
Sylvia T. Singer ◽  
Elliott P. Vichinsky ◽  
Ginny Gildengorin ◽  
Jereon van Disseldorp ◽  
Mitchell Rosen ◽  
...  
Keyword(s):  
Antral Follicle ◽  
Thalassemia Major ◽  
Antral Follicle Count ◽  
Reproductive Capacity ◽  
Gonadotropin Secretion ◽  
Ovarian Volume ◽  
Cardiac Iron ◽  
Labile Iron ◽  
Sensitive Marker

Abstract The pathophysiology of iron-induced compromised fertility in women with thalassemia major (TM) was evaluated in 26 adult TM females. Low gonadotropin secretion resulted in reduced ovarian antral follicle count and ovarian volume, but levels of anti-müllerian hormone (AMH), a sensitive marker for ovarian reserve independent of gonadotropin effect, were mostly normal. AMH correlated with non–transferrin-bound iron (NTBI), suggesting a role of labile iron in the pathogenesis of decreased reproductive capacity, possibly occurring in parallel to cardiac iron toxicity, as cardiac iron was associated with the presence of amenorrhea and with NTBI levels. AMH emerges as an important biomarker for assessment of reproductive capacity in TM, demonstrating that fertility is preserved in the majority of those younger than 30 to 35 years. AMH can be useful in future studies aiming at improved chelation for fertility preservation, whereas NTBI and labile plasma iron may be valuable for monitoring iron effect on the reproductive system.

scholarly journals SMAD1/5 Signaling in the Early Equine Placenta Regulates Trophoblast Differentiation and Chorionic Gonadotropin Secretion

Endocrinology ◽  
2014 ◽  
Vol 155 (8) ◽  
pp. 3054-3064 ◽  
Author(s):  
Victoria Cabrera-Sharp ◽  
Jordan E. Read ◽  
Stephanie Richardson ◽  
Alycia A. Kowalski ◽  
Douglas F. Antczak ◽  
...  
Keyword(s):  
Chorionic Gonadotropin ◽  
Trophoblast Cells ◽  
Rt Pcr ◽  
Trophoblast Differentiation ◽  
Gonadotropin Secretion ◽  
Morphogenetic Protein ◽  
Dose Dependent

TGFβ superfamily proteins, acting via SMAD (Sma- and Mad-related protein)2/3 pathways, regulate placental function; however, the role of SMAD1/5/8 pathway in the placenta is unknown. This study investigated the functional role of bone morphogenetic protein (BMP)4 signaling through SMAD1/5 in terminal differentiation of primary chorionic gonadotropin (CG)-secreting trophoblast. Primary equine trophoblast cells or placental tissues were isolated from day 27–34 equine conceptuses. Detected by microarray, RT-PCR, and quantitative RT-PCR, equine chorionic girdle trophoblast showed increased gene expression of receptors that bind BMP4. BMP4 mRNA expression was 20- to 60-fold higher in placental tissues adjacent to the chorionic girdle compared with chorionic girdle itself, suggesting BMP4 acts primarily in a paracrine manner on the chorionic girdle. Stimulation of chorionic girdle-trophoblast cells with BMP4 resulted in a dose-dependent and developmental stage-dependent increase in total number and proportion of terminally differentiated binucleate cells. Furthermore, BMP4 treatment induced non-CG-secreting day 31 chorionic girdle trophoblast cells to secrete CG, confirming a specific functional response to BMP4 stimulation. Inhibition of SMAD2/3 signaling combined with BMP4 treatment further enhanced differentiation of trophoblast cells. Phospho-SMAD1/5, but not phospho-SMAD2, expression as determined by Western blotting was tightly regulated during chorionic girdle trophoblast differentiation in vivo, with peak expression of phospho-SMAD1/5 in vivo noted at day 31 corresponding to maximal differentiation response of trophoblast in vitro. Collectively, these experiments demonstrate the involvement of BMP4-dependent pathways in the regulation of equine trophoblast differentiation in vivo and primary trophoblast differentiation in vitro via activation of SMAD1/5 pathway, a previously unreported mechanism of TGFβ signaling in the mammalian placenta.

scholarly journals Characterization of the Potent Luteinizing Hormone-Releasing Activity of KiSS-1 Peptide, the Natural Ligand of GPR54

Endocrinology ◽  
2005 ◽  
Vol 146 (1) ◽  
pp. 156-163 ◽  
Author(s):  
V. M. Navarro ◽  
J. M. Castellano ◽  
R. Fernández-Fernández ◽  
S. Tovar ◽  
J. Roa ◽  
...  
Keyword(s):  
Excitatory Amino Acid ◽  
Hypogonadotropic Hypogonadism ◽  
Mrna Levels ◽  
Central Administration ◽  
Experimental Conditions ◽  
Gonadotropin Secretion ◽  
Neuroendocrine Control ◽  
Lh Secretion

Loss-of-function mutations of the gene encoding GPR54, the putative receptor for the KiSS-1-derived peptide metastin, have been recently associated with hypogonadotropic hypogonadism, in both rodents and humans. Yet the actual role of the KiSS-1/GPR54 system in the neuroendocrine control of gonadotropin secretion remains largely unexplored. To initiate such analysis, the effects of KiSS-1 peptide on LH secretion were monitored using in vivo and in vitro settings under different experimental conditions. Central intracerebroventricular administration of KiSS-1 peptide potently elicited LH secretion in vivo over a range of doses from 10 pmol to 1 nmol. The effect of centrally injected KiSS-1 appeared to be mediated via the hypothalamic LHRH. However, no effect of central administration of KiSS-1 was detected on relative LHRH mRNA levels. Likewise, systemic (ip and iv) injection of KiSS-1 markedly stimulated LH secretion. This effect was similar in terms of maximum response to that of central administration of KiSS-1 and might be partially attributed to its ability to stimulate LH secretion directly at the pituitary. Finally, the LH-releasing activity of KiSS-1 was persistently observed after blockade of endogenous excitatory amino acid and nitric oxide pathways, i.e. relevant neurotransmitters in the neuroendocrine control of LH secretion. In summary, our results provide solid evidence for a potent stimulatory effect of KiSS-1 on LH release, acting at central levels (likely the hypothalamus) and eventually at the pituitary, and further document a novel role of the KiSS-1/GPR54 system as a relevant downstream element in the neuroendocrine network governing LH secretion.

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