Involvement of the corticotropin-releasing factor (CRF) type 2 receptor in CRF-induced thyrotropin release by the amphibian pituitary gland

Reiko Okada, Mark F. Miller, Kazutoshi Yamamoto, Bert De Groef, Robert J. Denver, Sakaé Kikuyama

    研究成果: Article

    37 引用 (Scopus)

    抄録

    Corticotropin-releasing factor (CRF) is considered to be a main adrenocorticotropin-releasing factor in vertebrates. In non-mammalian species, CRF and related peptides cause the release of thyroid-stimulating hormone (TSH) from the anterior pituitary. The actions of CRF peptides are mediated by two G protein coupled receptors (CRF1 and CRF2) that have different ligand specificities. Using ligands that bind preferentially or selectively to the CRF2 we tested the hypothesis that TSH release by the amphibian pituitary gland is mediated by the CRF2. Injection of frog CRF, urocortin 1 or the CRF2-specific ligand urocortin 3 all produced significant, acute increases (by 2 h) in plasma thyroxine concentration in prometamorphic tadpoles. Chronic injections of CRF peptides accelerated tadpole metamorphosis, and the peptides with the highest affinity for the CRF2 (urocortin 1 and sauvagine) had the greatest potency. Ligands selective for the CRF2 (frog urocortin 3, mouse urocortins 2 and 3) all accelerated tadpole metamorphosis. We then tested frog urocortins 1 and 3, mouse urocortin 2 and sauvagine for their TSH-releasing activity using dispersed frog anterior pituitary cells in culture. All of the peptides tested markedly enhanced the release of TSH. Secretagogue-induced TSH release was completely blocked by the general CRF receptor antagonist astressin or the CRF2-specific antagonist antisauvagine-30. Conversely, the type 1 CRF receptor-specific antagonist antalarmin had no effect on TSH secretion. Our results support the hypothesis that CRF-induced TSH release by the amphibian pituitary gland is mediated by the CRF2.

    元の言語English
    ページ(範囲)437-444
    ページ数8
    ジャーナルGeneral and Comparative Endocrinology
    150
    発行部数3
    DOI
    出版物ステータスPublished - 2007 2

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    corticotropin-releasing hormone
    Urocortins
    thyrotropin
    pituitary gland
    Corticotropin-Releasing Hormone
    Amphibians
    Pituitary Gland
    Thyrotropin
    amphibians
    receptors
    Anura
    peptides
    Peptides
    frogs
    Ligands
    tadpoles
    Larva
    antagonists
    anterior pituitary
    metamorphosis

    ASJC Scopus subject areas

    • Endocrinology

    これを引用

    Involvement of the corticotropin-releasing factor (CRF) type 2 receptor in CRF-induced thyrotropin release by the amphibian pituitary gland. / Okada, Reiko; Miller, Mark F.; Yamamoto, Kazutoshi; Groef, Bert De; Denver, Robert J.; Kikuyama, Sakaé.

    :: General and Comparative Endocrinology, 巻 150, 番号 3, 02.2007, p. 437-444.

    研究成果: Article

    Okada, Reiko ; Miller, Mark F. ; Yamamoto, Kazutoshi ; Groef, Bert De ; Denver, Robert J. ; Kikuyama, Sakaé. / Involvement of the corticotropin-releasing factor (CRF) type 2 receptor in CRF-induced thyrotropin release by the amphibian pituitary gland. :: General and Comparative Endocrinology. 2007 ; 巻 150, 番号 3. pp. 437-444.
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    abstract = "Corticotropin-releasing factor (CRF) is considered to be a main adrenocorticotropin-releasing factor in vertebrates. In non-mammalian species, CRF and related peptides cause the release of thyroid-stimulating hormone (TSH) from the anterior pituitary. The actions of CRF peptides are mediated by two G protein coupled receptors (CRF1 and CRF2) that have different ligand specificities. Using ligands that bind preferentially or selectively to the CRF2 we tested the hypothesis that TSH release by the amphibian pituitary gland is mediated by the CRF2. Injection of frog CRF, urocortin 1 or the CRF2-specific ligand urocortin 3 all produced significant, acute increases (by 2 h) in plasma thyroxine concentration in prometamorphic tadpoles. Chronic injections of CRF peptides accelerated tadpole metamorphosis, and the peptides with the highest affinity for the CRF2 (urocortin 1 and sauvagine) had the greatest potency. Ligands selective for the CRF2 (frog urocortin 3, mouse urocortins 2 and 3) all accelerated tadpole metamorphosis. We then tested frog urocortins 1 and 3, mouse urocortin 2 and sauvagine for their TSH-releasing activity using dispersed frog anterior pituitary cells in culture. All of the peptides tested markedly enhanced the release of TSH. Secretagogue-induced TSH release was completely blocked by the general CRF receptor antagonist astressin or the CRF2-specific antagonist antisauvagine-30. Conversely, the type 1 CRF receptor-specific antagonist antalarmin had no effect on TSH secretion. Our results support the hypothesis that CRF-induced TSH release by the amphibian pituitary gland is mediated by the CRF2.",
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    AU - Kikuyama, Sakaé

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