Role of Estradiol in the Dynamic Control of Tanycyte Plasticity Mediated by Vascular Endothelial Cells in the Median Eminence
Role of Estradiol in the Dynamic Control of Tanycyte Plasticity Mediated by Vascular Endothelial Cells in the Median Eminence
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DOI：
10.1210/en.2009-0870
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发表时间：
2010-04-01
期刊：
影响因子：
4.8
通讯作者：
Prevot, Vincent
中科院分区：
文献类型：
--
作者：
de Seranno, Sandrine;de Tassigny, Xavier d'Anglemont;Prevot, Vincent
在神经内分泌脑不断变化的生理背景下，涉及神经元、星形胶质细胞和血管细胞的细胞事件协调以产生适当的神经元信号的机制尚不清楚，但可以进行检查。在下丘脑的正中隆起，内皮细胞是伸长细胞（特化星形胶质细胞）可塑性和神经内分泌突触功效的关键参与者。在这里，我们报告，雌二醇作用于纯化的内皮细胞和分离的伸长细胞，触发内皮细胞与神经胶质细胞的通讯，导致伸长细胞过程的突然和大规模的收缩。通过体外腺病毒介导的内皮型一氧化氮合酶的显性阴性形式的基因转移阻断内皮型一氧化氮合酶，消除了内皮细胞介导的雌二醇诱导的伸展细胞可塑性。与此同时，由于暴露于雌二醇的伸长细胞诱导的环氧合酶（考克斯）-1和考克斯-2表达的变化，导致前列腺素E-2（PGE（2））增加，从而促进了伸长细胞的急性可塑性。我们还表明，通过电子显微镜，PGE 2的管理正中隆起外植体诱导快速神经胶质可塑性神经元的神经血管交界处释放GnRH（控制生殖的神经肽）。相反，用考克斯抑制剂消炎痛阻止成年雌性大鼠正中隆起的局部PGE 2合成会损害卵巢周期，这一过程需要将GnRH脉动、协调地递送到下丘脑-垂体门脉系统中。总之，我们的研究结果表明，雌二醇控制内皮细胞和星形胶质细胞之间的对话，以调节神经内分泌脑中的神经胶质细胞可塑性。（内分泌学151：1760-1772，2010）
In the ever-changing physiological context of the neuroendocrine brain, the mechanisms by which cellular events involving neurons, astroglia, and vascular cells are coordinated to bring forth the appropriate neuronal signaling is not yet known but is amenable to examination. In the median eminence of the hypothalamus, endothelial cells are key players in the plasticity of tanycytes (specialized astroglia) and neuroendocrine synapse efficacy. Here we report that estradiol acts on both purified endothelial cells and isolated tanycytes to trigger endothelial-to-glial communication that leads to a sudden and massive retraction of tanycyte processes. The blockade of endothelial nitric oxide synthase by in vitro adenoviral-mediated gene transfer of a dominant-negative form of endothelial nitric oxide synthase abrogates the estradiol-induced tanycyte plasticity mediated by endothelial cells. In parallel, increases in prostaglandin-E-2 (PGE(2)) due to changes in cyclooxygenase (COX)-1 and COX-2 expression induced by the exposure of tanycytes to estradiol promote acute tanycyte plasticity. We also demonstrate by electron microscopy that the administration of PGE2 to median eminence explants induces rapid neuroglial plasticity at the neurovascular junction of neurons that release GnRH (the neuropeptide controlling reproduction). Conversely, preventing local PGE2 synthesis in the median eminence of adult female rats with the COX inhibitor indomethacin impairs the ovarian cycle, a process that requires a pulsatile, coordinated delivery of GnRH into the hypothalamo-hypophyseal portal system. Taken together, our findings show that estradiol controls the dialog between endothelial cells and astroglia to regulate neuroglial plasticity in the neuroendocrine brain. (Endocrinology 151: 1760-1772, 2010)