étudie l’effet de la DHEA sur l’axe hypothalamo-hypophyso-ovarien Comme la . treatment results in suppression of the. hypothalamo-pituitary ovarian axis. Effet hypothalamo-hypophysaire: les antiprogestatifs ont aussi des effets plus ou moins Effets ovariens: si l’effet ovarien direct du RU est éliminé dans la qui ont des activités freinatrices sur l’axe hypothalamo-hypophyso-gonadique. Rôle de la signalisation des kisspeptines dans la régulation de l’axe nécessaires à l’activation centrale de l’axe hypothalamo-hypophyso-ovarien à la puberté.
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Mutations that interfere with kisspeptin signalling prevent normal pubertal development in humans and mice.
The role of kisspeptin signalling in ovarian physiology and placentation. The failure of the Gpr54 and Kiss1 mutant mice to ovulate has led to the suggestion that kisspeptin signalling may be required for the preovulatory luteinizing hormone LH surge.
EE Click here to see the Library ]. Hyppophyso is expressed in the AVPV region of the hypothalamus; an area known to regulate the pre-ovulatory LH surge in rodents. You may thus request that your data, should it be inaccurate, incomplete, unclear, outdated, not be used or stored, be corrected, clarified, updated or hypopyhso. Kisspeptins are hypopgyso series of overlapping peptides encoded by the Kiss1 gene that are required for central activation of the hypothalamic-pituitary-ovarian axis at puberty.
The role of kisspeptin signalling in the regulation of the GnRH-gonadotrophin ovarian axis in mice.
Nutrition et physiologie ovarienne.
Kisspeptin signalling is required for activation of the reproductive axis at puberty. We have found that mutant mice that have been induced to ovulate by injection of gonadotrophic hormones have lower progesterone levels than wild-type mice and we are investigating whether this represents an intrinsic defect in the corpus luteum.
Initial data indicate that pregnancy is not maintained in the mutant mice past day 7 of gestation even after hypotahlamo treatment. Access to the PDF text If you experience reading problems with Firefox, please follow this procedure. Kiss1 expression in AVPV neurons is increased in response to estradiol treatment and Kiss1 neurons are activated as indicated by c-fos induction. You can move this window by clicking on the headline. Mutant females do not show normal estrous cycling or ovulation.
We are investigating the causes of this failure to maintain pregnancy. Mutations in the kisspeptin receptor GPR54, cause infertility and hypogonadotrophic hypogonadism in humans. KiSS-1 in the mammalian ovary: Top of the page – Article Outline. Moderate kisspeptin is also found in regressing corpora lutea particularly in steroidogenic cells.
To investigate the effect that loss of both maternal and fetal kisspeptin signalling may have on placental function, we are restoring fertility to the mutant mice by hormone treatment and trying to establish pregnancy.
The role of kisspeptin signalling in the preovulatory LH surge. Access to the text HTML.
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Several lines of data support this hypothesis.
Regulator and marker of ovarian function E. Contact Help Who are we? The failure of the Gpr54 and Kiss1 mutant mice to ovulate has led to the suggestion that kisspeptin signalling may be required for the preovulatory surge. Although kisspeptin signalling has been shown to hypophyao an important central role in regulating the physiology of the ovary, the expression profile of Kiss1 and Gpr54 suggests that they may hypothalmao have direct functions in the ovary and the placenta.
Dramatic elevation of plasma metastin concentrations in human pregnancy: Hpyothalamo page Archives Sommaire. Personal information regarding our website’s visitors, including their identity, is confidential. Similarly, KISS1R immunoreactivity has been localized to the thecal layer of pre-ovulatory follicles and steroidogenic luteal cells of the corpus luteum.
Outline Masquer le plan. Expression of KiSS-1 in rat ovary: Physiologic roles and physiopathological implications M. The uteri are thread like and hypotthalamo ovaries significantly smaller than normal with no corpora lutea.
Expression of KISS1R by the highly invasive cytotrophoblast cells has led to the suggestion that these proteins may regulate placental invasion but the birth of Gpr54 and Kiss1 mutant mice indicates that placentation can take place in the absence of kisspeptin signalling from the fetal part of the placenta.