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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Membrane-initiated estradiol signaling induces spinogenesis required for female sexual receptivity.
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Membrane-initiated estradiol signaling induces spinogenesis required for female sexual receptivity.

机译：膜引发的雌二醇信号传导诱导女性性接受所需的自旋发生。

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摘要

Estrogens have profound actions on the structure of the nervous system during development and in adulthood. One of the signature actions of estradiol is to alter the morphology of neural processes. In the hippocampus, estradiol modulates spines and cellular excitability that affect cognitive behaviors. In the hypothalamus, estradiol increases spine density in mediobasal hypothalamic nuclei that regulate reproduction. The hypothalamic arcuate nucleus (ARH), an important site for modulation of female sexual receptivity, has a sexual dimorphism in dendritic spine density that favors females. In the present study, we used both beta-actin immunostaining and Golgi staining to visualize estradiol-induced changes in spine density in Long-Evans rats. Golgi impregnation was used to visualize spine shape, and then beta-actin immunoreactivity was used as a semiquantitative measure of spine plasticity since actin forms the core of dendritic spines. At 4 h after estradiol treatment, both beta-actin immunofluorescence and filopodial spines were increased (from 70.57 +/- 1.09% to 78.01 +/- 1.05%, p < 0.05). Disruption of estradiol-induced beta-actin polymerization with cytochalasin D attenuated lordosis behavior, indicating the importance of estradiol-mediated spinogenesis for female sexual receptivity (81.43 +/- 7.05 to 35.00 +/- 11.76, p < 0.05). Deactivation of cofilin, an actin depolymerizing factor is required for spinogenesis. Membrane-initiated estradiol signaling involving the metabotropic glutamate receptor 1a was responsible for the phosphorylation and thereby deactivation of cofilin. These data demonstrate that estradiol-induced spinogenesis in the ARH is an important cellular mechanism for the regulation of female sexual behavior.
机译：雌激素在发育和成年期对神经系统的结构具有深远的作用。雌二醇的标志性作用之一是改变神经过程的形态。在海马中，雌二醇调节刺和影响兴奋性的细胞兴奋性。在下丘脑中，雌二醇会增加调节生殖功能的下丘脑下丘脑核的脊柱密度。下丘脑弓状核（ARH）是调节女性性接受能力的重要部位，其树突棘密度具有性二态性，有利于女性。在本研究中，我们同时使用了β-肌动蛋白免疫染色和高尔基染色，以观察雌二醇诱导的Long-Evans大鼠脊柱密度的变化。高尔基浸渍法用于显示脊柱形状，然后将β-肌动蛋白免疫反应性用作脊柱可塑性的半定量指标，因为肌动蛋白形成树突棘的核心。雌二醇处理后4小时，β-肌动蛋白的免疫荧光和丝状棘都增加（从70.57 +/- 1.09％增至78.01 +/- 1.05％，p <0.05）。用细胞松弛素D破坏雌二醇诱导的β-肌动蛋白聚合可减弱脊柱前凸行为，表明雌二醇介导的自旋发生对于女性性接受性的重要性（81.43 +/- 7.05至35.00 +/- 11.76，p <0.05）。肌动蛋白解聚因子cofilin失活是自旋作用所必需的。涉及代谢型谷氨酸受体1a的膜引发的雌二醇信号传导负责磷酸化，从而使cofilin失活。这些数据表明雌激素诱导的ARH中的纺丝发生是调节女性性行为的重要细胞机制。

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