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首页> 外文期刊>The European Journal of Neuroscience >Oestrogen regulates sympathetic neurite outgrowth by modulating brain derived neurotrophic factor synthesis and release by the rodent uterus.
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Oestrogen regulates sympathetic neurite outgrowth by modulating brain derived neurotrophic factor synthesis and release by the rodent uterus.

机译：雌激素通过调节脑源性神经营养因子的合成和啮齿动物子宫的释放来调节交感神经突的生长。

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摘要

Sympathetic innervation of the adult rodent uterus undergoes cyclic remodelling. Terminal sympathetic axons degenerate when oestrogen levels rise and regenerate when oestrogen levels decline. This study examined the role of neurotrophins in oestrogen-mediated uterine sympathetic nerve remodelling. Oestrogen injection of ovariectomized female rats did not affect uterine NT-3 levels 24 h postinjection, and increased endometrial NGF protein, indicating that reduced NGF or NT-3 is not responsible for the oestrogen-induced denervation. Oestrogen also raised BDNF protein and mRNA in myometrium and endometrium. To assess whether increased BDNF affects uterine receptivity to sympathetic outgrowth, sympathetic ganglion explants were co-cultured with myometrium. Myometrium from ovariectomized rats induced neuritogenesis in oestrogen-free conditions, and this was abolished when BDNF was added to the medium. Neuritogenesis induced by ovariectomized myometrium was suppressed by oestrogen, and restored by a BDNF function-blocking antibody. To determine if target BDNF synthesis is required for oestrogen to suppress sympathetic neurite outgrowth, uteri from wild-type mice and mice homozygous or heterozygous for recombinant mutations of the BDNF gene were cultured with rat sympathetic ganglia. Neuritogenesis induced by wild-type uteri was diminished by oestrogen. Neurite formation in the presence of homozygous BDNF mutant uteri was not affected by oestrogen, but was lower than that of wild-type mice. Uteri from mice heterozygous for the BDNF mutation, who have reduced BDNF synthesis, showed normal neuritogenic properties, but were not affected by oestrogen. These findings suggest that oestrogen alters neuritogenic properties of the rodent uterus by regulating BDNF synthesis, which inhibits sympathetic neurite outgrowth.
机译：成年啮齿动物子宫的交感神经受周期性重塑。终末交感神经轴突在雌激素水平升高时退化，而在雌激素水平下降时再生。这项研究检查了神经营养蛋白在雌激素介导的子宫交感神经重塑中的作用。雌性卵巢切除的雌性大鼠注射后24小时并未影响子宫NT-3水平，也不增加子宫内膜NGF蛋白的含量，这表明NGF或NT-3的减少与雌激素引起的去神经作用无关。雌激素还增加了子宫内膜和子宫内膜的BDNF蛋白和mRNA。为了评估增加的BDNF是否会影响子宫对交感神经的容忍性，将交感神经节外植体与子宫肌层共培养。去卵巢大鼠的子宫肌层在无雌激素的条件下诱导了神经形成，当向培养基中添加BDNF时，这种情况就消失了。去卵巢子宫肌层诱导的神经发生被雌激素抑制，并被BDNF功能阻断抗体恢复。为了确定雌激素抑制交感神经突生长是否需要靶标BDNF合成，用大鼠交感神经节培养野生型小鼠的子宫和BDNF基因重组突变的纯合子或杂合子的子宫。雌激素可减少野生型子宫诱发的神经发生。在纯合子BDNF突变子宫的存在下，神经突的形成不受雌激素的影响，但低于野生型小鼠。 BDNF突变的杂合子小鼠的子宫，其BDNF合成减少，显示出正常的神经生成特性，但不受雌激素影响。这些发现表明，雌激素可通过调节BDNF合成来改变啮齿动物子宫的神经生成特性，从而抑制交感神经突的生长。

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