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  1. Article ; Online: The KiNG of reproduction: Kisspeptin/ nNOS interactions shaping hypothalamic GnRH release.

    Delli, Virginia / Silva, Mauro S B / Prévot, Vincent / Chachlaki, Konstantina

    Molecular and cellular endocrinology

    2021  Volume 532, Page(s) 111302

    Abstract: Gonadotropin-releasing hormone (GnRH) is the master regulator of the hypothalamic-pituitary-gonadal (HPG) axis, and therefore of fertility and reproduction. The release pattern of GnRH by the hypothalamus includes both pulses and surges. However, despite ...

    Abstract Gonadotropin-releasing hormone (GnRH) is the master regulator of the hypothalamic-pituitary-gonadal (HPG) axis, and therefore of fertility and reproduction. The release pattern of GnRH by the hypothalamus includes both pulses and surges. However, despite a considerable body of evidence in support of a determinant role for kisspeptin, the mechanisms regulating a GnRH pulse and surge remain a topic of debate. In this review we challenge the view of kisspeptin as an absolute "monarch", and instead present the idea of a Kisspeptin-nNOS-GnRH or "KiNG" network that is responsible for generating the "GnRH pulse" and "GnRH surge". In particular, the neuromodulator nitric oxide (NO) has opposite effects to kisspeptin on GnRH secretion in many respects, acting as the Yin to kisspeptin's Yang and creating a dynamic system in which kisspeptin provides the "ON" signal, promoting GnRH release, while NO mediates the "OFF" signal, acting as a tonic brake on GnRH secretion. This interplay between an activator and an inhibitor, which is in turn fine-tuned by the gonadal steroid environment, thus leads to the generation of GnRH pulses and surges and is crucial for the proper development and function of the reproductive axis.
    MeSH term(s) Animals ; Gonadotropin-Releasing Hormone/metabolism ; Humans ; Hypothalamus/metabolism ; Kisspeptins/metabolism ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type I/metabolism
    Chemical Substances KISS1 protein, human ; Kisspeptins ; Nitric Oxide (31C4KY9ESH) ; Gonadotropin-Releasing Hormone (33515-09-2) ; NOS1 protein, human (EC 1.14.13.39) ; Nitric Oxide Synthase Type I (EC 1.14.13.39)
    Language English
    Publishing date 2021-05-05
    Publishing country Ireland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 187438-x
    ISSN 1872-8057 ; 0303-7207
    ISSN (online) 1872-8057
    ISSN 0303-7207
    DOI 10.1016/j.mce.2021.111302
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1127: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article: The KiNG of reproduction: Kisspeptin/ nNOS interactions shaping hypothalamic GnRH release

    Delli, Virginia / Silva, Mauro S.B / Prévot, Vincent / Chachlaki, Konstantina

    Molecular and cellular endocrinology. 2021 July 15, v. 532

    2021  

    Abstract: Gonadotropin-releasing hormone (GnRH) is the master regulator of the hypothalamic-pituitary-gonadal (HPG) axis, and therefore of fertility and reproduction. The release pattern of GnRH by the hypothalamus includes both pulses and surges. However, despite ...

    Abstract Gonadotropin-releasing hormone (GnRH) is the master regulator of the hypothalamic-pituitary-gonadal (HPG) axis, and therefore of fertility and reproduction. The release pattern of GnRH by the hypothalamus includes both pulses and surges. However, despite a considerable body of evidence in support of a determinant role for kisspeptin, the mechanisms regulating a GnRH pulse and surge remain a topic of debate. In this review we challenge the view of kisspeptin as an absolute “monarch”, and instead present the idea of a Kisspeptin-nNOS-GnRH or “KiNG” network that is responsible for generating the “GnRH pulse” and “GnRH surge”. In particular, the neuromodulator nitric oxide (NO) has opposite effects to kisspeptin on GnRH secretion in many respects, acting as the Yin to kisspeptin's Yang and creating a dynamic system in which kisspeptin provides the “ON” signal, promoting GnRH release, while NO mediates the “OFF” signal, acting as a tonic brake on GnRH secretion. This interplay between an activator and an inhibitor, which is in turn fine-tuned by the gonadal steroid environment, thus leads to the generation of GnRH pulses and surges and is crucial for the proper development and function of the reproductive axis.
    Keywords gonadotropin-releasing hormone ; gonads ; hypothalamus ; kisspeptin ; nitric oxide ; reproduction
    Language English
    Dates of publication 2021-0715
    Publishing place Elsevier B.V.
    Document type Article
    ZDB-ID 187438-x
    ISSN 1872-8057 ; 0303-7207
    ISSN (online) 1872-8057
    ISSN 0303-7207
    DOI 10.1016/j.mce.2021.111302
    Database NAL-Catalogue (AGRICOLA)

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    Zs.A 1127: Show issues Location:
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  3. Article ; Online: Male minipuberty involves the gonad-independent activation of preoptic nNOS neurons.

    Delli, Virginia / Dehame, Julien / Franssen, Delphine / Rasika, S / Parent, Anne-Simone / Prevot, Vincent / Chachlaki, Konstantina

    Free radical biology & medicine

    2022  

    Abstract: Background: The maturation of the hypothalamic-pituitary-gonadal (HPG) axis is crucial for the establishment of reproductive function. In female mice, neuronal nitric oxide synthase (nNOS) activity appears to be key for the first postnatal activation of ...

    Abstract Background: The maturation of the hypothalamic-pituitary-gonadal (HPG) axis is crucial for the establishment of reproductive function. In female mice, neuronal nitric oxide synthase (nNOS) activity appears to be key for the first postnatal activation of the neural network promoting the release of gonadotropin-releasing hormone (GnRH), i.e. minipuberty. However, in males, the profile of minipuberty as well as the role of nNOS-expressing neurons remain unexplored.
    Methods: nNOS-deficient and wild-type mice were studied during postnatal development. The expression of androgen (AR) and estrogen receptor alpha (ERα) as well as nNOS phosphorylation were evaluated by immunohistochemistry in nNOS neurons in the median preoptic nucleus (MePO), where most GnRH neuronal cell bodies reside, and the hormonal profile of nNOS-deficient male mice was assessed using previously established radioimmunoassay and ELISA methods. Gonadectomy and pharmacological manipulation of ERα were used to elucidate the mechanism of minipubertal nNOS activation and the maturation of the HPG axis.
    Results: In male mice, minipubertal FSH release occurred at P23, preceding the LH surge at P30, when balanopreputial separation occurs. Progesterone and testosterone remained low during minipuberty, increasing around puberty, whereas estrogen levels were high throughout postnatal development. nNOS neurons showed a sharp increase in Ser
    Conclusions: Our results show that the timing of minipuberty differs in male mice when compared to females, but as in the latter, nNOS activity in the preoptic region plays a role in this process. Additionally, akin to male non-human primates, the profile of minipuberty in male mice is shaped by sex-independent mechanisms, and possibly involves extragonadal estrogen sources.
    Language English
    Publishing date 2022-12-02
    Publishing country United States
    Document type Journal Article
    ZDB-ID 807032-5
    ISSN 1873-4596 ; 0891-5849
    ISSN (online) 1873-4596
    ISSN 0891-5849
    DOI 10.1016/j.freeradbiomed.2022.11.040
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2109: Show issues Location:
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  4. Article ; Online: Female sexual behavior is disrupted in a preclinical mouse model of PCOS via an attenuated hypothalamic nitric oxide pathway.

    Silva, Mauro S B / Decoster, Laurine / Trova, Sara / Mimouni, Nour E H / Delli, Virginia / Chachlaki, Konstantina / Yu, Qiang / Boehm, Ulrich / Prevot, Vincent / Giacobini, Paolo

    Proceedings of the National Academy of Sciences of the United States of America

    2022  Volume 119, Issue 30, Page(s) e2203503119

    Abstract: Women with polycystic ovary syndrome (PCOS) frequently experience decreased sexual arousal, desire, and sexual satisfaction. While the hypothalamus is known to regulate sexual behavior, the specific neuronal pathways affected in patients with PCOS are ... ...

    Abstract Women with polycystic ovary syndrome (PCOS) frequently experience decreased sexual arousal, desire, and sexual satisfaction. While the hypothalamus is known to regulate sexual behavior, the specific neuronal pathways affected in patients with PCOS are not known. To dissect the underlying neural circuitry, we capitalized on a robust preclinical animal model that reliably recapitulates all cardinal PCOS features. We discovered that female mice prenatally treated with anti-Müllerian hormone (PAMH) display impaired sexual behavior and sexual partner preference over the reproductive age. Blunted female sexual behavior was associated with increased sexual rejection and independent of sex steroid hormone status. Structurally, sexual dysfunction was associated with a substantial loss of neuronal nitric oxide synthase (nNOS)-expressing neurons in the ventromedial nucleus of the hypothalamus (VMH) and other areas of hypothalamic nuclei involved in social behaviors. Using in vivo chemogenetic manipulation, we show that nNOS
    MeSH term(s) Animals ; Anti-Mullerian Hormone/pharmacology ; Disease Models, Animal ; Female ; Mating Preference, Animal ; Mice ; Neurons/drug effects ; Neurons/enzymology ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type I/genetics ; Nitric Oxide Synthase Type I/metabolism ; Polycystic Ovary Syndrome/enzymology ; Polycystic Ovary Syndrome/physiopathology ; Sexual Behavior ; Ventromedial Hypothalamic Nucleus/drug effects ; Ventromedial Hypothalamic Nucleus/metabolism
    Chemical Substances Nitric Oxide (31C4KY9ESH) ; Anti-Mullerian Hormone (80497-65-0) ; Nitric Oxide Synthase Type I (EC 1.14.13.39) ; Nos1 protein, mouse (EC 1.14.13.39)
    Language English
    Publishing date 2022-07-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2203503119
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1148: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  5. Article ; Online: Multi- and Transgenerational Outcomes of an Exposure to a Mixture of Endocrine-Disrupting Chemicals (EDCs) on Puberty and Maternal Behavior in the Female Rat.

    López-Rodríguez, David / Aylwin, Carlos Francisco / Delli, Virginia / Sevrin, Elena / Campanile, Marzia / Martin, Marion / Franssen, Delphine / Gérard, Arlette / Blacher, Silvia / Tirelli, Ezio / Noël, Agnès / Lomniczi, Alejandro / Parent, Anne-Simone

    Environmental health perspectives

    2021  Volume 129, Issue 8, Page(s) 87003

    Abstract: Background: The effects of endocrine-disrupting chemicals (EDCs) on fertility and reproductive development represent a rising concern in modern societies. Although the neuroendocrine control of sexual maturation is a major target of EDCs, little is ... ...

    Abstract Background: The effects of endocrine-disrupting chemicals (EDCs) on fertility and reproductive development represent a rising concern in modern societies. Although the neuroendocrine control of sexual maturation is a major target of EDCs, little is known about the potential role of the hypothalamus in puberty and ovulation disruption transmitted across generations.
    Objectives: We hypothesized that developmental exposure to an environmentally relevant dose of EDC mixture could induce multi- and/or transgenerational alterations of sexual maturation and maternal care in female rats through epigenetic reprograming of the hypothalamus. We investigated the transmission of a disrupted reproductive phenotype via the maternal germline or via nongenomic mechanisms involving maternal care.
    Methods: Adult female Wistar rats were exposed prior to and during gestation and until the end of lactation to a mixture of the following 13 EDCs: di-
    Results: Germ cell (F2) and transgenerationally (F3) EDC-exposed females, but not F1, displayed delayed pubertal onset and altered folliculogenesis. We reported a transgenerational alteration of key hypothalamic genes controlling puberty and ovulation (
    Discussion: Rats developmentally exposed to an EDC mixture exhibited multi- and transgenerational disruption of sexual maturation and maternal care via hypothalamic epigenetic reprogramming. These results raise concerns about the impact of EDC mixtures on future generations. https://doi.org/10.1289/EHP8795.
    MeSH term(s) Animals ; Endocrine Disruptors/toxicity ; Epigenesis, Genetic ; Female ; Hypothalamus/drug effects ; Maternal Behavior/drug effects ; Pregnancy ; Prenatal Exposure Delayed Effects/chemically induced ; Rats ; Rats, Wistar ; Sexual Maturation
    Chemical Substances Endocrine Disruptors
    Language English
    Publishing date 2021-08-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 195189-0
    ISSN 1552-9924 ; 0091-6765 ; 1078-0475
    ISSN (online) 1552-9924
    ISSN 0091-6765 ; 1078-0475
    DOI 10.1289/EHP8795
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.B 1360: Show issues Location:
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    Zs.MO 379: Show issues

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  6. Article ; Online: GnRH neurons recruit astrocytes in infancy to facilitate network integration and sexual maturation.

    Pellegrino, Giuliana / Martin, Marion / Allet, Cécile / Lhomme, Tori / Geller, Sarah / Franssen, Delphine / Mansuy, Virginie / Manfredi-Lozano, Maria / Coutteau-Robles, Adrian / Delli, Virginia / Rasika, S / Mazur, Danièle / Loyens, Anne / Tena-Sempere, Manuel / Siepmann, Juergen / Pralong, François P / Ciofi, Philippe / Corfas, Gabriel / Parent, Anne-Simone /
    Ojeda, Sergio R / Sharif, Ariane / Prevot, Vincent

    Nature neuroscience

    2021  Volume 24, Issue 12, Page(s) 1660–1672

    Abstract: Neurons that produce gonadotropin-releasing hormone (GnRH), which control fertility, complete their nose-to-brain migration by birth. However, their function depends on integration within a complex neuroglial network during postnatal development. Here, ... ...

    Abstract Neurons that produce gonadotropin-releasing hormone (GnRH), which control fertility, complete their nose-to-brain migration by birth. However, their function depends on integration within a complex neuroglial network during postnatal development. Here, we show that rodent GnRH neurons use a prostaglandin D
    MeSH term(s) Astrocytes/metabolism ; Gonadotropin-Releasing Hormone/metabolism ; Hypothalamus/physiology ; Neurons/physiology ; Sexual Maturation/physiology
    Chemical Substances Gonadotropin-Releasing Hormone (33515-09-2)
    Language English
    Publishing date 2021-11-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1420596-8
    ISSN 1546-1726 ; 1097-6256
    ISSN (online) 1546-1726
    ISSN 1097-6256
    DOI 10.1038/s41593-021-00960-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 4891: Show issues Location:
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    Zs.MG 67: Show issues

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  7. Article ; Online: NOS1

    Chachlaki, Konstantina / Messina, Andrea / Delli, Virginia / Leysen, Valerie / Maurnyi, Csilla / Huber, Chieko / Ternier, Gaëtan / Skrapits, Katalin / Papadakis, Georgios / Shruti, Sonal / Kapanidou, Maria / Cheng, Xu / Acierno, James / Rademaker, Jesse / Rasika, Sowmyalakshmi / Quinton, Richard / Niedziela, Marek / L'Allemand, Dagmar / Pignatelli, Duarte /
    Dirlewander, Mirjam / Lang-Muritano, Mariarosaria / Kempf, Patrick / Catteau-Jonard, Sophie / Niederländer, Nicolas J / Ciofi, Philippe / Tena-Sempere, Manuel / Garthwaite, John / Storme, Laurent / Avan, Paul / Hrabovszky, Erik / Carleton, Alan / Santoni, Federico / Giacobini, Paolo / Pitteloud, Nelly / Prevot, Vincent

    Science translational medicine

    2022  Volume 14, Issue 665, Page(s) eabh2369

    Abstract: The nitric oxide (NO) signaling pathway in hypothalamic neurons plays a key role in the regulation of the secretion of gonadotropin-releasing hormone (GnRH), which is crucial for reproduction. We hypothesized that a disruption of neuronal NO synthase ( ... ...

    Abstract The nitric oxide (NO) signaling pathway in hypothalamic neurons plays a key role in the regulation of the secretion of gonadotropin-releasing hormone (GnRH), which is crucial for reproduction. We hypothesized that a disruption of neuronal NO synthase (NOS1) activity underlies some forms of hypogonadotropic hypogonadism. Whole-exome sequencing was performed on a cohort of 341 probands with congenital hypogonadotropic hypogonadism to identify ultrarare variants in
    MeSH term(s) Animals ; Cognition ; Gonadotropin-Releasing Hormone/genetics ; Gonadotropin-Releasing Hormone/metabolism ; Humans ; Hypogonadism/complications ; Hypogonadism/congenital ; Hypogonadism/genetics ; Mice ; Mutant Proteins ; Mutation/genetics ; Nitric Oxide ; Nitric Oxide Synthase Type I/genetics ; Nitrites
    Chemical Substances Mutant Proteins ; Nitrites ; Nitric Oxide (31C4KY9ESH) ; Gonadotropin-Releasing Hormone (33515-09-2) ; NOS1 protein, human (EC 1.14.13.39) ; Nitric Oxide Synthase Type I (EC 1.14.13.39) ; Nos1 protein, mouse (EC 1.14.13.39)
    Language English
    Publishing date 2022-10-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2518854-9
    ISSN 1946-6242 ; 1946-6234
    ISSN (online) 1946-6242
    ISSN 1946-6234
    DOI 10.1126/scitranslmed.abh2369
    Database MEDical Literature Analysis and Retrieval System OnLINE

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