Radial glia express aromatase in the injured zebra finch brain
Radial glia express aromatase in the injured zebra finch brain
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DOI：
10.1002/cne.20157
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发表时间：
2004-07-19
影响因子：
2.5
通讯作者：
Schlinger, BA
中科院分区：
文献类型：
--
作者：
Peterson, RS;Lee, DW;Schlinger, BA
雌激素具有神经营养和神经保护特性。雌激素的合成通过芳香酶的表达发生。先前的研究表明，脊椎动物脑损伤导致病变周围星形胶质细胞中芳香化酶表达的快速和显著上调。作为研究损伤诱导的神经胶质芳构化的实验的一部分，我们确定了斑胸草雀脑放射状神经胶质中的芳构化酶。成年雌性斑胸草雀右侧海马体受到穿透性损伤。损伤后24小时，给鸟施用溴脱氧尿苷（BrdU），并在2小时、1天或7天后处死。用免疫细胞化学方法测定芳香化酶和BrdU标记的分布。放射状芳香化酶定位于邻近受损海马的侧脑室内衬细胞。损伤还诱导了新产生的细胞与BrdU标记的病变周围的戏剧性积累。BrdU标记与芳香化酶阳性放射状纤维密切相关，表明新产生的细胞沿着这些纤维迁移。在鸣禽的大脑中，雌激素支持神经元的募集，促进新神经元的存活和增加。放射状胶质细胞中芳香化酶的存在提供了雌激素传递到有丝分裂后细胞的机制。放射状芳构化可能是神经损伤后脊椎动物脑修复的关键特征。(C)2004年Wiley-Liss，Inc.
Estrogens have neurotrophic and neuroprotective properties. The synthesis of estrogen occurs via the expression of aromatase. Previous studies have shown that injury to the vertebrate brain results in a rapid and dramatic up-regulation of aromatase expression in astrocytes around the lesion. As part of experiments examining injury-induced glial aromatization, we identified aromatase in radial glia of the zebra finch brain. Adult female zebra finches received a penetrating injury to the right hippocampus. Twenty-four hours after lesioning, birds were administered bromodeoxyuridine (BrdU) and sacrificed 2 hours, 1 day, or 7 days later. We determined the distribution of aromatase and BrdU labeling by using immunocytochemistry. Radial aromatase was localized to cells lining the lateral ventricle adjacent to the lesioned hippocampus. Injury also induced a dramatic accumulation of newly generated cells labeled with BrdU around the lesion. BrdU labeling was strongly associated with aromatase-positive radial fibers, suggesting the migration of newly generated cells along these fibers. In the songbird brain, estrogen supports neuronal recruitment and promotes the survival and addition of new neurons. The presence of aromatase in radial glia provides a mechanism of estrogen delivery to postmitotic cells. Radial aromatization may be a key feature in the repair of the vertebrate brain following neural injury. (C) 2004 Wiley-Liss, Inc.