GONADOTROPHIN-RELEASING HORMONE DEFICIENCY IN A MUTANT MOUSE WITH HYPOGONADISM
GONADOTROPHIN-RELEASING HORMONE DEFICIENCY IN A MUTANT MOUSE WITH HYPOGONADISM
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DOI：
10.1038/269338a0
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发表时间：
1977-01-01
期刊：
影响因子：
64.8
通讯作者：
FINK, G
中科院分区：
文献类型：
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作者：
CATTANACH, BM;IDDON, CA;FINK, G
由于单独的促性腺激素分泌缺乏，人类家族性性腺功能减退症已被充分证实1 -6，但由于缺乏合适的动物模型4而难以研究。我们在这里报告的遗传和内分泌背景的突变品系的小鼠，其中睾丸和卵巢未能发展产后。其主要原因似乎是下丘脑促性腺激素释放激素（GnRH）缺乏，导致垂体含量和促黄体生成激素（LH）和促卵泡激素（FSH）循环水平降低。通过与Brattleboro大鼠（加压素合成中的遗传缺陷）类比，该突变体应被证明可用于研究下丘脑释放激素的合成以及下丘脑促性腺激素系统在性分化、青春期、卵泡发生和精子发生中的作用。该突变体被命名为性腺功能减退，符号hpg。
FAMILIAL hypogonadism in man, due to an isolated deficiency of gonadotrophin secretion, has been well documented1–6, but difficult to investigate because of the lack of a suitable animal model4. We report here the genetic and endocrinological background of a mutant strain of mouse in which the testes and ovaries fail to develop postnatally. The primary cause of this seems to be a deficiency in hypothalamic gonadotrophin-releasing hormone (GnRH) with a consequent reduction in pituitary content and circulating levels of luteinising hormone (LH) and follicle-stimulating hormone (FSH). By analogy with the Brattleboro rat (genetic defect in vasopressin synthesis) this mutant should prove useful for studying the synthesis of hypothalamic releasing hormones as well as the role of the hypothalamic–gonadotrophin system in sexual differentiation, puberty, folliculogenesis and spermatogenesis. The mutant has been named hypogonadal, symbolhpg.