Reversal of reproductive deficiency in the hpg male mouse by neonatal androgenization.
Reversal of reproductive deficiency in the hpg male mouse by neonatal androgenization.
复制标题
通过新生雄激素化逆转 HPG 雄性小鼠的生殖缺陷。
DOI：
10.1095/biolreprod47.4.561
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发表时间：
1992
影响因子：
3.6
通讯作者：
Gibson,MJ
中科院分区：
文献类型：
--
作者：
Livne,I;Silverman,AJ;Gibson,MJ
通过将含有 GnRH 细胞的正常胎儿脑组织移植到成年 hpg 小鼠的中枢神经系统中，可以恢复 GnRH 缺陷性性腺功能减退 (hpg) 突变小鼠的生殖功能的某些方面。然而，对移植物表现出生理反应的hpg雄性无法表现出性行为并且不育。我们假设这些男性的生殖缺陷是由于 GnRH 缺乏导致围产期睾丸雄激素暴露不足所致。为了验证这一假设，我们通过给新生儿注射丙酸睾酮（TP）来使雄性雄性激素产生雄激素。对照组由新生儿未雄激素化的 HPG 雄性和正常雄性组成。所有三组在成年后都接受了 TP 植入，并记录了他们的交配行为和生殖能力。此外，其他未在新生儿中雄激素化的hpg雄性接受了含有GnRH神经元的胎儿脑移植，并在接受TP植入之前和之后测试了交配行为和生殖能力。8只新生儿雄激素化hpg雄性中的3只表现出了男性性行为的全部技能，包括插入和射精，并生下了几窝幼仔。 7只在新生儿时没有雄激素化但在成年后接受TP植入的对照雄性雄性中的3只也表现出勃起和性交，但没有射精的证据，并且这些雄性未能使正常雌性受孕。在对胎儿移植有睾丸生长反应的 8 只雄性雄性动物中，只有 1 只表现出骑乘行为。然而，当给予TP植入物时，移植的8hpg雄性中有4只表现出安装和插入。我们得出结论，交配行为雄性化所需的围产期雄激素在hpg小鼠中缺乏，因此可能依赖于GnRH分泌。因此，成年雄性小鼠的生殖行为的充分表达必须依赖于下丘脑-垂体-性腺轴的功能。
Some aspects of reproductive function in the GnRH-deficient hypogonadal (hpg) mutant mouse can be restored by transplanting normal fetal brain tissue containing GnRH cells into the central nervous system of adulthpgmice. However,hpgmales showing physiological response to the graft fail to display sexual behavior and are infertile. We hypothesized that the reproductive deficit of these males is due to insufficient perinatal exposure to testicular androgens as a consequence of the GnRH deficiency. To test this hypothesis we androgenizedhpgmales by giving them neonatal injections of testosterone propionate (TP). Controls consisted ofhpgmales not androgenized neonatally and of normal males. All three groups received a TP implant in adulthood, and their copulatory behavior and reproductive capability were recorded. In addition, otherhpgmales, not androgenized neonatally, received fetal brain transplants containing GnRH neurons and were also tested for copulatory behavior and reproductive capability before and after receiving a TP implant.Three of 8 neonatally androgenizedhpgmales expressed the full repertoire of male sexual behavior, including intromission and ejaculation, and sired several litters. Three of 7 controlhpgmales that were not androgenized neonatally but received TP implants in adulthood also displayed mounting and intromission, but there was no evidence of ejaculation, and these males failed to impregnate normal females. Of the 8hpgmales that responded to a fetal transplant with testicular growth, only 1 displayed mounting behavior. However, when given a TP implant, 4 of 8hpgmales with grafts displayed mounting and intromissions.We conclude that perinatal androgens, which are required to masculinize copulatory behavior, are deficient in thehpgmouse and therefore are probably dependent on GnRH secretion. Accordingly, full expression of adult reproductive behavior must be dependent on a functional hypothalamic-pituitary-gonadal axis in the neonatal male mouse.