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本文引用的文献

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Presumptive Estrogen Target Neurons Express mRNAs for both the Neurotrophins and Neurotrophin Receptors: A Basis for Potential Developmental Interactions of Estrogen with the Neurotrophins.推定雌激素靶神经元表达神经营养因子及其受体的 mRNAs:雌激素与神经营养因子潜在发育相互作用的基础。
Mol Cell Neurosci. 1993 Dec;4(6):510-25. doi: 10.1006/mcne.1993.1063.
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Immunocytochemical investigation of nuclear progestin receptor expression within dopaminergic neurones of the female rat brain.雌性大鼠脑内多巴胺能神经元中核孕激素受体表达的免疫细胞化学研究。
J Neuroendocrinol. 2004 Jun;16(6):534-43. doi: 10.1111/j.1365-2826.2004.01198.x.
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Progestin receptors: neuronal integrators of hormonal and environmental stimulation.孕激素受体:激素与环境刺激的神经元整合器
Ann N Y Acad Sci. 2003 Dec;1007:238-50. doi: 10.1196/annals.1286.023.
4
Minireview: A plethora of estrogen receptors in the brain: where will it end?综述:大脑中大量的雌激素受体:这将走向何方?
Endocrinology. 2004 Mar;145(3):1069-74. doi: 10.1210/en.2003-1462. Epub 2003 Dec 11.
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Differential effects of progestins on the brain.孕激素对大脑的不同作用。
Maturitas. 2003 Dec 10;46 Suppl 1:S71-5. doi: 10.1016/j.maturitas.2003.09.021.
6
Oestrogen regulates sympathetic neurite outgrowth by modulating brain derived neurotrophic factor synthesis and release by the rodent uterus.雌激素通过调节啮齿动物子宫中脑源性神经营养因子的合成与释放来调控交感神经轴突的生长。
Eur J Neurosci. 2003 Nov;18(10):2760-8. doi: 10.1111/j.1460-9568.2003.03029.x.
7
Plasticity in developing rat uterine sensory nerves: the role of NGF and TrkA.发育中大鼠子宫感觉神经的可塑性:神经生长因子(NGF)和酪氨酸激酶受体A(TrkA)的作用
Cell Tissue Res. 2003 Nov;314(2):191-205. doi: 10.1007/s00441-003-0799-9. Epub 2003 Sep 13.
8
Reduced age-related plasticity of neurotrophin receptor expression in selected sympathetic neurons of the rat.大鼠特定交感神经元中神经营养因子受体表达的年龄相关性可塑性降低。
Aging Cell. 2003 Feb;2(1):59-69. doi: 10.1046/j.1474-9728.2003.00035.x.
9
The oestrogenized rat myometrium inhibits organotypic sympathetic reinnervation.雌激素化的大鼠子宫肌层会抑制器官型交感神经再支配。
Auton Neurosci. 2002 Oct 31;101(1-2):13-22. doi: 10.1016/s1566-0702(02)00173-x.
10
Continuous infusion of neurotrophin-3 triggers sprouting, decreases the levels of TrkA and TrkC, and inhibits epileptogenesis and activity-dependent axonal growth in adult rats.持续输注神经营养因子-3可引发轴突发芽,降低成年大鼠中TrkA和TrkC的水平,并抑制癫痫发生及活动依赖性轴突生长。
Neuroscience. 2002;115(4):1295-308. doi: 10.1016/s0306-4522(02)00384-6.

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.

DOI:10.1111/j.1469-7580.2005.00435.x
PMID:16050899
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1571519/
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。