Gonadotropin-releasing hormone agonist affects rat ovarian follicle development by interfering with FSH and growth factors on the prevention of apoptosis

2001 ◽  
Vol 60 (2) ◽  
pp. 241-247 ◽  
Author(s):  
F. Parborell ◽  
L. Dain ◽  
M. Tesone
Keyword(s):  
Growth Factors ◽  
Ovarian Follicle ◽  
Gonadotropin Releasing Hormone ◽  
Follicle Development ◽  
Releasing Hormone ◽  
Ovarian Follicle Development ◽  
Gonadotropin Releasing Hormone Agonist

Effect of Luteinizing Hormone-Releasing Hormone Analogs on the Rat Ovarian Follicle Development

1997 ◽  
Vol 48 (3) ◽  
pp. 35-41 ◽  
Author(s):  
Tetsu Yano ◽  
Naomi Yano ◽  
Hirotaka Matsumi ◽  
Yutaka Morita ◽  
Osamu Tsutsumi ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Ovarian Follicle ◽  
Follicle Development ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Ovarian Follicle Development ◽  
Hormone Analogs

Lleyn breed is likely source of BMP15 and GDF9 mutations, that have large effects on ovulation rate, discovered in Cambridge and Belclare breeds

2007 ◽  
Vol 2007 ◽  
pp. 4-4
Author(s):  
J. P. Hanrahan ◽  
M. Mullen
Keyword(s):  
Growth Factors ◽  
Litter Size ◽  
Ovarian Follicle ◽  
Genetic Material ◽  
Point Mutations ◽  
Common Source ◽  
Follicle Development ◽  
Major Contributor ◽  
Chromosome 5 ◽  
Ovarian Follicle Development

Exceptionally high prolificacy in the Cambridge and Belclare breeds has been shown to be attributable to point mutations in genes (BMP15 and GDF9) that code for oocyte derived growth factors which have profound effects on ovarian follicle development. The BMP15 gene is X linked while GDF9 is autosomal (chromosome 5). Two different BMP15 mutations are present in the Belclare population (FecXG and FecXB) but only one of these (FecXG) was found in the Cambridge while the GDF9 mutation (FecGH) was common to both breeds. The Inverdale and Hanna mutations in NZ Romney sheep (Davis et al. 2001) are point mutations in BMP15 but involve different codons from those involved in Cambridge and Belclare. It is of interest to know whether the mutations common to Cambridge and Belclare are likely to have had a common ancestral source or arose independently. The Lleyn breed was a common source of genetic material in the genesis of both breeds. Thus, the foundation ewes for the Cambridge included three Lleyn ewes (Owen,1976) while a set of 13 Lleyn sheep selected for high litter size was a major contributor to the Belclare breed (accounted for 50% of the genetic material at one stage; subsequently diluted to about 25%). The hypothesis is that the Lleyn was the likely source of the two mutations common to Belclare and Cambridge.

Growth Factors in Normal Ovarian Follicle Development

1996 ◽  
Vol 14 (03) ◽  
pp. 179-196 ◽  
Author(s):  
Linda Giudice ◽  
Nicholas Cataldo ◽  
H.J.H.M. van Vessel ◽  
O.W. Yap ◽  
Yasmin Chandrasekher
Keyword(s):  
Growth Factors ◽  
Ovarian Follicle ◽  
Follicle Development ◽  
Ovarian Follicle Development

scholarly journals Addition of a carboxy terminal tail to the normally tailless gonadotropin-releasing hormone receptor impairs fertility in female mice

2021 ◽  
Author(s):  
Chirine Toufaily ◽  
Jerome Fortin ◽  
Carlos A.I. Alonso ◽  
Evelyne Lapointe ◽  
Xiang Zhou ◽  
...  
Keyword(s):  
Ovarian Follicle ◽  
Selective Advantage ◽  
Gonadotropin Releasing Hormone ◽  
Lh Surge ◽  
Releasing Hormone ◽  
Ovarian Follicle Development ◽  
Carboxy Terminal ◽  
Gonadotropin Releasing Hormone Receptor ◽  
G Protein Coupled ◽  
Homologous Desensitization

Gonadotropin-releasing hormone (GnRH) is the primary neuropeptide controlling reproduction in vertebrates. GnRH stimulates follicle-stimulating hormone (FSH) and luteinizing hormone (LH) synthesis via a G protein-coupled receptor, GnRHR, in the pituitary gland. In mammals, GnRHR lacks a C-terminal cytosolic tail (Ctail) and does not exhibit homologous desensitization. This might be an evolutionary adaptation that enables LH surge generation and ovulation. To test this idea, we fused the chicken GnRHR Ctail to the endogenous murine GnRHR in a transgenic model. The LH surge was blunted, but not blocked in these mice. In contrast, they showed reductions in FSH production, ovarian follicle development, and fertility. Addition of the Ctail altered the nature of agonist-induced calcium signaling required for normal FSH production. The loss of the GnRHR Ctail during mammalian evolution is unlikely to have conferred a selective advantage by enabling the LH surge. The adaptive significance of this specialization remains to be determined.

scholarly journals Addition of a carboxy terminal tail to the normally tailless gonadotropin-releasing hormone receptor impairs fertility in female mice

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Chirine Toufaily ◽  
Jérôme Fortin ◽  
Carlos AI Alonso ◽  
Evelyne Lapointe ◽  
Xiang Zhou ◽  
...  
Keyword(s):  
Ovarian Follicle ◽  
Selective Advantage ◽  
Gonadotropin Releasing Hormone ◽  
Lh Surge ◽  
Releasing Hormone ◽  
Ovarian Follicle Development ◽  
Carboxy Terminal ◽  
Gonadotropin Releasing Hormone Receptor ◽  
G Protein Coupled ◽  
Homologous Desensitization

Gonadotropin-releasing hormone (GnRH) is the primary neuropeptide controlling reproduction in vertebrates. GnRH stimulates follicle-stimulating hormone (FSH) and luteinizing hormone (LH) synthesis via a G protein-coupled receptor, GnRHR, in the pituitary gland. In mammals, GnRHR lacks a C-terminal cytosolic tail (Ctail) and does not exhibit homologous desensitization. This might be an evolutionary adaptation that enables LH surge generation and ovulation. To test this idea, we fused the chicken GnRHR Ctail to the endogenous murine GnRHR in a transgenic model. The LH surge was blunted, but not blocked in these mice. In contrast, they showed reductions in FSH production, ovarian follicle development, and fertility. Addition of the Ctail altered the nature of agonist-induced calcium signaling required for normal FSH production. The loss of the GnRHR Ctail during mammalian evolution is unlikely to have conferred a selective advantage by enabling the LH surge. The adaptive significance of this specialization remains to be determined.

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