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大鼠子宫交感神经的可塑性:TrkA和p75神经生长因子受体的作用。

Plasticity in rat uterine sympathetic nerves: the role of TrkA and p75 nerve growth factor receptors.

作者信息

Richeri Analía, Bianchimano Paola, Mármol Nelson M, Viettro Lorena, Cowen Timothy, Brauer M Mónica

机构信息

Laboratorio de Biología Celular, Instituto de Investigaciones Biológicas Clemente Estable, Montevideo, Uruguay.

出版信息

J Anat. 2005 Aug;207(2):125-34. doi: 10.1111/j.1469-7580.2005.00435.x.

Abstract

Uterine sympathetic innervation undergoes profound remodelling in response to physiological and experimental changes in the circulating levels of sex hormones. It is not known, however, whether this plasticity results from changes in the innervating neurons, the neuritogenic properties of the target tissue or both. Using densitometric immunohistochemistry, we analysed the effects of prepubertal chronic oestrogen treatment (three subcutaneous injections of 20 microg of beta-oestradiol 17-cypionate on days 25, 27 and 29 after birth), natural peripubertal transition and late pregnancy (19-20 days post coitum) on the levels of TrkA and p75 nerve growth factor receptors in uterine-projecting sympathetic neurons of the thoraco-lumbar paravertebral sympathetic chain (T7-L2) identified using the retrograde tracer Fluorogold. For comparative purposes, levels of TrkA and p75 were assessed in the superior cervical ganglion (SCG) following prepubertal chronic oestrogen treatment. These studies showed that the vast majority of uterine-projecting neurons expressed both TrkA and p75. Both prepubertal chronic oestrogen treatment and the peripubertal transition increased the ratio p75 to TrkA in uterine-projecting neurons, whereas pregnancy elicited the opposite effect. Prepubertal chronic oestrogen treatment had no effects on levels of TrkA or p75 in sympathetic neurons of the SCG. Taken together, our data suggest that neurotrophin receptor-mediated events may contribute to regulate sex hormone-induced plasticity in uterine sympathetic nerves, and are in line with the idea that, in vivo, plasticity in uterine nerves involves changes in both the target and the innervating neurons.

摘要

子宫交感神经支配会因循环性激素水平的生理和实验性变化而发生深刻重塑。然而,尚不清楚这种可塑性是由支配神经元的变化、靶组织的神经发生特性的变化还是两者共同作用导致的。我们使用密度测定免疫组织化学方法,分析了青春期前慢性雌激素处理(出生后第25、27和29天皮下注射三次20微克17-β-雌二醇环戊丙酸酯)、自然青春期过渡和妊娠晚期(交配后19 - 20天)对使用逆行示踪剂荧光金标记的胸腰段椎旁交感神经链(T7 - L2)中投射至子宫的交感神经元中TrkA和p75神经生长因子受体水平的影响。为作比较,我们还评估了青春期前慢性雌激素处理后颈上神经节(SCG)中TrkA和p75的水平。这些研究表明,绝大多数投射至子宫的神经元同时表达TrkA和p75。青春期前慢性雌激素处理和青春期过渡均增加了投射至子宫的神经元中p75与TrkA的比值,而妊娠则产生相反的效果。青春期前慢性雌激素处理对SCG交感神经元中TrkA或p75的水平没有影响。综上所述,我们的数据表明神经营养因子受体介导的事件可能有助于调节性激素诱导的子宫交感神经可塑性,这与体内子宫神经可塑性涉及靶组织和支配神经元两者变化的观点一致。

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