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Sex differences in the hypothalamic-pituitary-adrenal axis: Roles of estrogen receptor-beta in the adult female rat brain.

机译：下丘脑-垂体-肾上腺轴的性别差异：成年雌性大鼠脑中雌激素受体-β的作用。

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摘要

In animals and humans, the hypothalamic-pituitary-adrenal (HPA) axis represents the major neuroendocrine axis responding to stress. Interestingly, a sex difference exists in HPA function in response to stress, where females exhibit a more robust response than males. Previous studies have shown that this sex difference is at least partly due to the differences in circulating levels of estrogen. The purpose of this project was to reveal the mechanisms of estrogen action in enhancing the activity of HPA axis. In the present studies, we have demonstrated the presence of estrogen receptor-beta (ER-β) in neurons that express corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP), the two important regulators of the HPA axis, in the paraventricular (PVN) and supraoptic (SON) nuclei of the female rat hypothalamus. These findings may represent one mechanism by which estrogen directly increases tone of the two key HPA regulators. This may further underlie the reported gender differences in the HPA response to stress. In addition, it is shown that ER-β is differentially regulated by estrogen vs. glucocorticoids. Estrogen down-regulates, while glucocorticoids up-regulate, ER-β immunoreactivity and mRNA levels in the hypothalamus. Since changes in ER-β concentrations in a given cell could influence its sensitivity to estrogen signals, ER-β autologous down-regulation by estrogen in neurons of the PVN and SON will likely to suppress estrogen sensitivity of these neurons. In contrast, increases in cellular ER-β levels in response to exposure to glucocorticoids will likely enhance cellular sensitivity to estrogen. In light of reports showing that estrogen increases the expression of CRH and AVP in the rodent hypothalamus, an increase in the ER-β protein by glucocorticoids could therefore potentiate activational properties of estrogen on HPA function following chronic glucocorticoid receptor activation. Thus, an additional mechanism underlying the known sex difference in HPA regulation might be through up-regulation of ER-β by stress-elevated levels of glucocorticoids. Taken together, these findings help to define a picture of how estrogen participates in the enhancement of HPA function following stress. This may provide a foundation for further research into the roles of estrogen in a reported sex difference in stress response.
机译：在动物和人类中，下丘脑-垂体-肾上腺（HPA）轴代表响应压力的主要神经内分泌轴。有趣的是，在对压力的反应中，HPA功能存在性别差异，女性表现出比男性更强壮的反应。先前的研究表明，这种性别差异至少部分是由于雌激素循环水平的差异所致。该项目的目的是揭示雌激素作用增强HPA轴活性的机制。在本研究中，我们已经证明了在室旁表达表达促肾上腺皮质激素释放激素（CRH）和精氨酸加压素（AVP）（HPA轴的两个重要调节因子）的神经元中存在雌激素受体β（ER-β）。雌性大鼠下丘脑的（PVN）和超视（SON）核。这些发现可能代表了一种雌激素直接增加两个关键HPA调节剂音调的机制。这可能进一步解释了所报告的HPA对压力反应的性别差异。另外，显示ER-β受雌激素相对于糖皮质激素的差异调节。雌激素下调，而糖皮质激素上调，下丘脑中的ER-β免疫反应性和mRNA水平。由于给定细胞中ER-β浓度的变化可能会影响其对雌激素信号的敏感性，因此，PVN和SON神经元中雌激素引起的ER-β自体下调可能会抑制这些神经元的雌激素敏感性。相反，响应于暴露于糖皮质激素的细胞中ER-β水平的升高可能会增强细胞对雌激素的敏感性。鉴于有报道显示雌激素会增加啮齿类动物下丘脑中CRH和AVP的表达，因此糖皮质激素使ER-β蛋白增加可能会增强慢性糖皮质激素受体激活后雌激素对HPA功能的激活特性。因此，HPA调节中已知性别差异背后的另一种机制可能是通过糖皮质激素的应激水平上调ER-β。综上所述，这些发现有助于确定雌激素在压力后如何参与增强HPA功能。这可能为进一步研究雌激素在压力反应中报道的性别差异中的作用提供基础。

著录项

  • 作者

    Suzuki, Shotaro.;

  • 作者单位

    Loyola University of Chicago.;

  • 授予单位 Loyola University of Chicago.;
  • 学科 Biology Neuroscience.; Biology Molecular.
  • 学位 Ph.D.
  • 年度 2003
  • 页码 212 p.
  • 总页数 212
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 神经科学;分子遗传学;
  • 关键词

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