Neuroendocrine and reproductive functions in male mice with targeted disruption of the prolactin gene.
Neuroendocrine and reproductive functions in male mice with targeted disruption of the prolactin gene.
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DOI：
10.1210/endo.139.9.6209
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发表时间：
1998-09
期刊：
影响因子：
4.8
通讯作者：
Richard W. Steger;V. Chandrashekar;W. Zhao;A. Bartke;N. Horseman
中科院分区：
文献类型：
--
作者：
Richard W. Steger;V. Chandrashekar;W. Zhao;A. Bartke;N. Horseman
使用具有PRL基因的靶向破坏（敲除）的小鼠（PRL-KO）来研究PRL在控制与生殖相关的雄性神经内分泌功能中的生理作用。与正常雄性相比，PRL-KO小鼠的中位隆起多巴胺含量、血浆LH水平、体外LH和FSH分泌（每mg垂体）以及精囊和腹侧前列腺重量均显著降低。PRL是没有检测到在孵育培养基与垂体从PRL基因敲除小鼠。在有或没有LH的情况下，在PRL-KO小鼠中未检测到中位隆起去甲肾上腺素、血浆睾酮水平或体外睾酮释放（每mg睾丸）的变化。在从与正常雌性小鼠一起饲养直至受孕的时间间隔内，在PRL-KO与正常雄性小鼠中未检测到差异，妊娠率或每窝活仔数。PRL-KO小鼠的泌乳素重量增加（1.78 +/- 0.22对3.35 +/- 0.20 mg; P < 0.001），推测是由于反馈抑制减少以及非功能性催乳细胞的肥大和/或增生。这些结果表明，PRL的缺乏减少垂体LH的释放，减弱正中隆起多巴胺能活性，并影响精囊和腹侧前列腺的生长。虽然它以前表明，PRL可以修复雄性垂体侏儒小鼠的生殖缺陷，我们目前的研究结果表明，PRL缺乏单独是不足以导致男性不育，虽然有明显的改变，在生殖神经内分泌功能的PRL基因敲除男性。
Mice with a targeted disruption (knock-out) of the PRL gene (PRL-KO) were used to study the physiological role of PRL in the control of male neuroendocrine functions related to reproduction. Compared with normal males, PRL-KO mice had significant reductions in median eminence dopamine content, plasma LH levels, LH and FSH secretion in vitro (per mg pituitary), and weights of seminal vesicles and ventral prostate. PRL was not detectable in incubation medium with pituitaries from PRL-KO mice. No alterations were detected in PRL-KO mice in median eminence norepinephrine, plasma testosterone levels, or testosterone release (per mg testis) in vitro with or without LH. No differences were detected in PRL-KO vs. normal male mice in the interval from housing with normal female mice until conception, rate of pregnancy, or the number of live pups per litter. Pituitary weight in PRL-KO mice was increased (1.78 +/- 0.22 vs. 3.35 +/- 0.20 mg; P < 0.001), presumably due to reduced feedback inhibition and hypertrophy and/or hyperplasia of nonfunctional lactotrophs. These results indicate that the absence of PRL reduces pituitary LH release, attenuates median eminence dopaminergic activity, and affects the growth of seminal vesicles and ventral prostate. Although it was previously shown that PRL can repair the reproductive defect in male pituitary dwarf mice, our current results imply that the PRL deficiency alone is not sufficient to cause male infertility, although there are obvious alterations in reproductive neuroendocrine function in PRL-KO males.