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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Hypothhalamo data indicate that pregnancy is not maintained in the mutant mice past day 7 of gestation even after progesterone treatment. Several lines of data support this hypothesis.
You may thus request that your data, should it be inaccurate, incomplete, unclear, outdated, not be used or stored, be corrected, clarified, updated or deleted. Kisspeptin signalling is required for activation of the reproductive axis at puberty.
Mutations in the kisspeptin receptor GPR54, cause infertility and hypogonadotrophic hypogonadism in humans. Journal page Archives Sommaire. Dramatic elevation of plasma metastin concentrations in human pregnancy: Physiologic roles and physiopathological implications M.
Kiss1 is expressed in the AVPV region of the hypothalamus; an area hypophhyso to regulate the pre-ovulatory LH surge in rodents.
Although kisspeptin signalling has been shown to have an important central role in regulating the physiology of the ovary, the expression profile of Kiss1 and Gpr54 suggests that they may also have direct functions in the ovary and the placenta. Similarly, KISS1R immunoreactivity has been localized to the thecal layer of pre-ovulatory follicles and steroidogenic luteal cells of the corpus luteum.
Top of the page – Article Outline. Regulator and marker of ovarian function E. Access to the PDF text If you experience reading problems with Firefox, please follow this procedure. Expression of KiSS-1 in rat ovary: You can move this window by clicking on the headline.
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Nutrition et physiologie ovarienne.
The role of kisspeptin signalling in the preovulatory LH surge. Outline Masquer le plan. Access to the text HTML. The failure of the Gpr54 and Kiss1 mutant mice to ovulate has led to the suggestion hypophgso kisspeptin signalling may be required for the preovulatory luteinizing hormone LH surge.
The role of kisspeptin signalling in the regulation of the GnRH-gonadotrophin ovarian axis in mice. The role of kisspeptin signalling in ovarian physiology and placentation. We are investigating the causes of this failure to maintain pregnancy.
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Mutant females do not show normal estrous cycling or ovulation.
Moderate kisspeptin is also found in regressing corpora lutea particularly in steroidogenic cells. 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.
Personal information regarding our website’s visitors, including their identity, is confidential. EE Click here to see the Library ]. 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.
The uteri are thread like and the ovaries significantly smaller than normal with no corpora lutea. 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. Mutations that interfere with kisspeptin signalling prevent normal pubertal development in humans and mice. KiSS-1 in the mammalian ovary: Kisspeptins are a series of overlapping peptides encoded by the Kiss1 gene that are required for central activation of the hypothalamic-pituitary-ovarian axis at puberty.
Contact Help Who are we? Kiss1 expression in AVPV neurons is increased in response to estradiol treatment and Kiss1 neurons are activated as indicated by c-fos induction. 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.