Nongenomic mechanism mediates estradiol stimulation of axon growth in male rat hypothalamic neurons in vitro
Nongenomic mechanism mediates estradiol stimulation of axon growth in male rat hypothalamic neurons in vitro
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非基因组机制介导体外雌二醇刺激雄性大鼠下丘脑神经元轴突生长
DOI：
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发表时间：
2001
影响因子：
4.2
通讯作者：
H. Carrer
中科院分区：
文献类型：
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作者：
M. Cambiasso;H. Carrer
本工作的目的是研究雌二醇受体（ER）在体外雌激素诱导的轴突生长中的参与。将来自 16 天 (E16) 雄性大鼠胎儿的下丘脑神经元在基础培养基或由腹侧中脑 (CM) 衍生的星形胶质细胞调节的培养基中培养，含或不含 1 × 10-7 M 17-β-雌二醇。体外48小时后，通过形态测量分析对神经突生长进行量化。添加到 CM 中的雌二醇可以证明轴原效应。通过 RT-PCR，在供体组织以及神经元培养物中发现了 ERα 的 mRNA 转录本。在该模型中，两种特定的核 ER 阻滞剂（他莫昔芬和 ICI 182,780）无法有效阻断致神经突效应，而膜不可渗透的雌激素-白蛋白结构 (E2-BSA) 与雌二醇一样有效。这些结果表明雌二醇在 E16 处的轴原作用不是通过经典的细胞内受体信号转导系统发挥的，并表明膜介导机制的可能性。根据我们之前的发现讨论了这些数据，这些发现指出介导刺激的轴突生长的雌激素和营养因子信号通路的相互依赖的激活。 J.神经科学。资源。 66:475–481, 2001。© 2001 Wiley-Liss, Inc.
The purpose of the present work was to investigate the participation of estradiol receptors (ER) in estrogen‐induced axon growth in vitro. Hypothalamic neurons from 16 day (E16) male rat fetuses were cultured with or without 17‐β‐estradiol at 1 × 10–7 M in basal medium or medium conditioned by astroglia derived from ventral mesencephalon (CM). After 48 hr in vitro, neurite outgrowth was quantified by morphometric analysis. An axogenic effect could be demonstrated for estradiol added to CM. With RT‐PCR, the mRNA transcript for ERα was found in the donor tissues as well as in the neuron cultures. In this model two specific nuclear ER blockers (tamoxifen and ICI 182,780) were ineffective in blocking the neuritogenic effect, and a membrane‐impermeable estrogen–albumin construct (E2‐BSA) was as effective as estradiol. These results indicate that the axogenic effect of estradiol at E16 is not exerted through the classical intracellular receptor signal transduction system and suggest the possibility of a membrane‐mediated mechanism. The data are discussed in light of our previous findings pointing to the interdependent activation of the estrogenic and the trophic factor signaling pathways that mediate stimulated axon growth. J. Neurosci. Res. 66:475–481, 2001. © 2001 Wiley‐Liss, Inc.
影响因子：
4.8
作者：
J. Watters;J. S. Campbell;M. Cunningham;E. Krebs;D. Dorsa
通讯作者：
J. Watters;J. S. Campbell;M. Cunningham;E. Krebs;D. Dorsa
影响因子：
4.8
作者：
Yue Zhou;J. Watters;D. Dorsa
通讯作者：
Yue Zhou;J. Watters;D. Dorsa
影响因子：
4
作者：
Moats, RK;Ramirez, VD
通讯作者：
Ramirez, VD