Vascular endothelial cells promote acute plasticity in ependymoglial cells of the neuroendocrine brain
Vascular endothelial cells promote acute plasticity in ependymoglial cells of the neuroendocrine brain
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DOI：
10.1523/jneurosci.3228-04.2004
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发表时间：
2004-11-17
影响因子：
5.3
通讯作者：
Prevot, V
中科院分区：
文献类型：
--
作者：
De Seranno, S;Estrella, C;Prevot, V
神经胶质细胞和内皮细胞在整个大脑中相互作用，以定义特定的功能区。内皮细胞是否将信号传递给成熟大脑中的神经胶质细胞尚不清楚，但可以在脑室周围器官进行检查。在这里，我们报道了这些器官之一的纯化内皮细胞，即下丘脑的正中隆起，在分离的室管膜神经胶质细胞中诱导急性肌动蛋白细胞骨架重塑，并表明这种可塑性是由一氧化氮(NO)介导的，一氧化氮是一种扩散因子。我们发现，可溶性鸟苷酸环化酶和环氧合酶产物都参与了这种内皮介导的室管膜胶质细胞结构的调控。我们还通过电子显微镜证明，正中隆起内源性NO释放的激活导致结构的快速变化，使含有促性腺激素释放激素(GnRH)(控制生殖功能的神经肽)的神经分泌轴突直接进入门静脉血管。体内局部抑制NO合成会破坏生殖循环，这一过程需要将GnRH脉动、协调地输送到下丘脑-腺垂体门脉系统。我们的结果确认了内皮细胞在诱导神经胶质可塑性方面以前未知的功能，并提出了整个大脑的内皮细胞可能使用类似的信号机制来调节神经胶质-神经元相互作用的有趣可能性。
Glial and endothelial cells interact throughout the brain to define specific functional domains. Whether endothelial cells convey signals to glia in the mature brain is unknown but is amenable to examination in circumventricular organs. Here we report that purified endothelial cells of one of these organs, the median eminence of the hypothalamus, induce acute actin cytoskeleton remodeling in isolated ependymoglial cells and show that this plasticity is mediated by nitric oxide (NO), a diffusible factor. We found that both soluble guanylyl cyclase and cyclooxygenase products are involved in this endothelial-mediated control of ependymoglia cytoarchitecture. We also demonstrate by electron microscopy that activation of endogenous NO release in the median eminence induces rapid structural changes, allowing a direct access of neurosecretory axons containing gonadotropin-releasing hormone (GnRH) (the neuropeptide controlling reproductive function) to the portal vasculature. Local in vivo inhibition of NO synthesis disrupts reproductive cyclicity, a process that requires a pulsatile, coordinated delivery of GnRH into the hypothalamic-adenohypophyseal portal system. Our results identify a previously unknown function for endothelial cells in inducing neuroglial plasticity and raise the intriguing possibility that endothelial cells throughout the brain may use a similar signaling mechanism to regulate glial-neuronal interactions.