Prostaglandin E2 induces glutamate release from subventricular zone astrocytes
Prostaglandin E2 induces glutamate release from subventricular zone astrocytes
复制标题
DOI：
10.1017/s1740925x10000244
复制
发表时间：
2010-01-01
影响因子：
--
通讯作者：
Bordey, Angelique
中科院分区：
文献类型：
--
作者：
Dave, Kathleen A.;Platel, Jean-Claude;Bordey, Angelique
最近有报道称，在成年神经发生区之一的脑室下区(SVZ)，星形胶质细胞样细胞在细胞内钙离子升高时释放谷氨酸。然而，控制SVZ星形胶质细胞钙活性和谷氨酸释放的信号尚不清楚。在这里，我们研究了诱导成熟星形胶质细胞释放谷氨酸的前列腺素E2(PGE2)是否就是这样的信号。利用膜片钳技术，我们证明了神经母细胞中N-甲基-D-天冬氨酸受体(NMDAR)通道的活性是环境谷氨酸水平的高保真传感器。使用这种传感器，我们发现PGE2的应用导致了SVZ中环境谷氨酸水平的增加。在平行实验中，PGE2诱导SVZ细胞，特别是星形胶质细胞样细胞内钙水平增加，如钙成像所示。最后，PGE2酶免疫分析显示侧脑室的脉络丛和较小程度的SVZ(少10倍)释放PGE2。这些发现表明，PGE2是一种生理信号，可以诱导SVZ星形胶质细胞释放谷氨酸，而谷氨酸释放对控制神经母细胞的存活和增殖是重要的。这一信号可能在缺血或损伤诱导的PGE2释放后增强，并可能参与损伤相关的神经发生增加。
It was recently reported that in one of the adult neurogenetic zones, the subventricular zone (SVZ), astrocyte-like cells release glutamate upon intracellular Ca2+ increases. However, the signals that control Ca2+ activity and glutamate release from SVZ astrocytes are not known. Here, we examined whether prostaglandin E2 (PGE2), which induces glutamate release from mature astrocytes, is such a signal. Using the gramicidin-perforated patch-clamp technique, we show that the activity of N-Methyl-D-Aspartate receptor (NMDAR) channel in neuroblasts is a high fidelity sensor of ambient glutamate levels. Using such sensors, we found that application of PGE2 led to increased ambient glutamate levels in the SVZ. In parallel experiments, PGE2 induced an increase in intracellular Ca2+ levels in SVZ cells, in particular astrocyte-like cells, as shown using Ca2+ imaging. Finally, a PGE2 enzyme immunoassay showed that the choroid plexus of the lateral ventricle and to a lesser extent the SVZ (ten-fold less) released PGE2. These findings suggest that PGE2 is a physiological signal for inducing glutamate release from SVZ astrocytes that is important for controlling neuroblast survival and proliferation. This signal may be accentuated following ischemia or injury-induced PGE2 release and may contribute to the injury-associated increased neurogenesis.