Universidad Europea de Madrid, Department of Psychology, Calle Tajo s/n, 28670 Villaviciosa de Odon, Madrid, Spain; Neuroscience Institute Cavalieri Ottolenghi (NICO), Regione Gonzole 10, 10043 Orbassano, Italy; Universidad Nacional de Educacion a Distancia (UNED), Department of Psychobiology, Calle Juan del Rosal 10, 28040 Madrid, Spain.
University of Turin, Department of Neuroscience, via Cherasco 15, 10126 Turin, Italy; Neuroscience Institute Cavalieri Ottolenghi (NICO), Regione Gonzole 10, 10043 Orbassano, Italy.
Brain Res. 2019 Jun 1;1712:93-100. doi: 10.1016/j.brainres.2019.02.002. Epub 2019 Feb 4.
The ovarian hormone 17β-estradiol is known to regulate the release, expression and immunoreactivity of arginine-vasopressin (AVP) in the supraoptic and paraventricular hypothalamic nuclei of rodents. Previous studies have shown that estrogen receptor α is involved in the effects of chronic estradiol administration on arginine-vasopressin immunoreactivity in the female rat hypothalamus. In this study we have examined the effect of an acute administration of estradiol or specific agonists for estrogen receptors α, β and G protein-coupled estrogen receptor 1 on the immunoreactivity of arginine-vasopressin in the hypothalamus of adult ovariectomized female rats. Acute estradiol administration resulted in a significant decrease in the number of arginine-vasopressin immunoreactive neurons in the supraoptic and paraventricular nuclei after 24 h. The effects of the specific estrogen receptors agonists suggest that the action of estradiol on arginine-vasopressin immunoreactivity is mediated in the supraoptic nucleus by G protein-coupled estrogen receptor 1 and in the paraventricular nucleus by both estrogen receptor β and G protein-coupled estrogen receptor 1. Thus, in contrast to previous studies on the effect of chronic estrogenic treatments, the present findings suggest that estrogen receptor β and G protein-coupled estrogen receptor 1 mediate the acute effects of estradiol on arginine-vasopressin immunoreactivity in the hypothalamus of ovariectomized rats.
卵巢激素 17β-雌二醇已知可调节啮齿动物的视上核和室旁核中精氨酸血管加压素 (AVP) 的释放、表达和免疫反应性。先前的研究表明,雌激素受体 α 参与了雌激素对雌性大鼠下丘脑精氨酸血管加压素免疫反应性的慢性给药的影响。在这项研究中,我们检查了急性给予雌二醇或雌激素受体 α、β 和 G 蛋白偶联雌激素受体 1 的特异性激动剂对成年去卵巢雌性大鼠下丘脑精氨酸血管加压素免疫反应性的影响。急性雌二醇给药 24 小时后,视上核和室旁核中精氨酸血管加压素免疫反应性神经元的数量明显减少。特定雌激素受体激动剂的作用表明,雌二醇对精氨酸血管加压素免疫反应性的作用是由 G 蛋白偶联雌激素受体 1 在视上核中介导的,由雌激素受体 β 和 G 蛋白偶联雌激素受体 1 在室旁核中介导的。因此,与慢性雌激素治疗作用的先前研究相反,本研究结果表明,雌激素受体 β 和 G 蛋白偶联雌激素受体 1 介导了去卵巢大鼠下丘脑精氨酸血管加压素免疫反应性的雌二醇的急性作用。