Estrogen and female reproductive tract innervation: cellular and molecular mechanisms of autonomic neuroplasticity.
Estrogen and female reproductive tract innervation: cellular and molecular mechanisms of autonomic neuroplasticity.
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DOI：
10.1016/j.autneu.2014.11.009
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发表时间：
2015-01
影响因子：
2.7
通讯作者：
Smith, Peter G.
中科院分区：
文献类型：
--
作者：
Brauer, M. Monica;Smith, Peter G.
关键词：
女性生殖道经历了显着的功能和结构的变化与周期，概念和怀孕，它可能是有利的个人和物种，以改变生殖组织和神经支配之间的关系。几十年来，人们已经认识到，哺乳动物子宫在妊娠后期经历了大量的交感神经轴突耗竭，这可能代表了一种适应，以促进平滑肌静止和持续的血流。子宫颈和阴道等其他结构的神经支配也会发生与妊娠相关的神经支配变化，这可能有助于分娩。这些组织为研究周围神经系统可塑性的细胞和分子机制提供了高度易处理的模型。研究表明，雌激素可促进子宫肌层交感神经终末轴突的快速变性，而后者在低雌激素条件下可再生。变性由靶组织介导：在雌激素的影响下，子宫肌层产生排斥交感神经轴突的蛋白质，包括BDNF、神经三蛋白、脑信号蛋白和神经生长因子原，并且细胞外基质成分被重塑。有趣的是，神经耗竭并不涉及促进轴突生长的经典交感神经营养因子水平的降低。雌激素还影响交感神经元神经营养因子受体的表达，其方式似乎有利于靶组织的促变性作用。与子宫相反，雌激素消耗阴道自主神经和伤害性轴突，后者部分由雌激素诱导的抑制BMP 4合成驱动。这些研究结果表明，神经介导的生理可塑性是一个高度复杂的现象，涉及多个，主要是排斥性的目标衍生的因素，在一致行动，以实现快速和选择性减少神经支配。
The female reproductive tract undergoes remarkable functional and structural changes associated with cycling, conception and pregnancy, and it is likely advantageous to both individual and species to alter relationships between reproductive tissues and innervation. For several decades, it has been appreciated that the mammalian uterus undergoes massive sympathetic axon depletion in late pregnancy, possibly representing an adaptation to promote smooth muscle quiescence and sustained blood flow. Innervation to other structures such as cervix and vagina also undergo pregnancy-related changes in innervation that may facilitate parturition. These tissues provide highly tractable models for examining cellular and molecular mechanisms underlying peripheral nervous system plasticity. Studies show that estrogen elicits rapid degeneration of sympathetic terminal axons in myometrium, which regenerate under low-estrogen conditions. Degeneration is mediated by the target tissue: under estrogen's influence, the myometrium produces proteins repulsive to sympathetic axons including BDNF, neurotrimin, semaphorins, and pro-NGF, and extracellular matrix components are remodeled. Interestingly, nerve depletion does not involve diminished levels of classical sympathetic neurotrophins that promote axon growth. Estrogen also affects sympathetic neuron neurotrophin receptor expression in ways that appear to favor pro-degenerative effects of the target tissue. In contrast to the uterus, estrogen depletes vaginal autonomic and nociceptive axons, with the latter driven in part by estrogen-induced suppression BMP4 synthesis. These findings illustrate that hormonally mediated physiological plasticity is a highly complex phenomenon involving multiple, predominantly repulsive target-derived factors acting in concert to achieve rapid and selective reductions in innervation.
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DOI：
10.1016/s0165-1838(99)00094-6
发表时间：
2000-02-14
期刊：
JOURNAL OF THE AUTONOMIC NERVOUS SYSTEM
影响因子：
--
作者：
Brauer, MM;Shockley, KP;Crutcher, KA
通讯作者：
Crutcher, KA
影响因子：
15.1
作者：
Arnold, Julia;de Arellano, Maria L. Barcena;Mechsner, Sylvia
通讯作者：
Mechsner, Sylvia
影响因子：
3.4
作者：
Al-Shawi, Raya;Hafner, Angela;Cowen, Timothy
通讯作者：
Cowen, Timothy
影响因子：
6.1
作者：
Al-Jefout, M.;Dezarnaulds, G.;Fraser, I. S.
通讯作者：
Fraser, I. S.
影响因子：
3
作者：
ALBUQUERQUEARAUJO, WIC;ROSAESILVA, AAM;FAVARETTO, ALV
通讯作者：
FAVARETTO, ALV