GDNF induces synaptic vesicle markers in enteric neurons
GDNF induces synaptic vesicle markers in enteric neurons
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DOI：
10.1016/j.neures.2013.08.012
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发表时间：
2013-11-01
影响因子：
2.9
通讯作者：
Wedel, T.
中科院分区：
文献类型：
--
作者：
Boettner, M.;Harde, J.;Wedel, T.
肠运动的调节依赖于完整的突触囊泡装置。因此，我们研究了突触囊泡标记物突触素和突触小泡蛋白在人肠神经系统（ENS）和它们的调节胶质细胞源性神经营养因子（GDNF）在培养的肠neurons.Full厚度标本的人结肠的突触素和突触小泡蛋白的表达和神经元定位进行了评估，通过双标记免疫细胞化学与PGP 9.5。GDNF对两种突触标记物的影响进行了监测，在肠神经细胞培养和静脉曲张的存在下，通过应用电子显微镜的culture.Human结肠标本显示在肌间和粘膜下神经节，以及在神经纤维的突触素和synaptobrevin的免疫反应。两种突触囊泡标记物共同GDNF与神经元标记物PGP 9.5定位，并在人和大鼠ENS中表现出颗粒积聚模式。在培养的大鼠肌间神经元中，GDNF处理促进突触囊泡标记物的表达和神经元静脉曲张的形成。GDNF对肠神经元中突触泡蛋白和突触小泡蛋白的调节表明，在培养中诱导功能性神经元网络的特征在于增加了神经元的突触泡蛋白和突触小泡蛋白的表达。突触发生的过程(C)2013 Elsevier爱尔兰有限公司和日本神经科学学会。All rights reserved.
Regulation of intestinal motility depends on an intact synaptic vesicle apparatus. Thus, we investigated the expression of the synaptic vesicle markers synaptophysin and synaptobrevin in the human enteric nervous system (ENS) and their regulation by glial cell line-derived neurotrophic factor (GDNF) in cultured enteric neurons.Full-thickness specimens of the human colon were assessed for expression of synaptophysin and synaptobrevin and neuronal localization was assessed by dual-label immunocytochemistry with PGP 9.5. Effects of GDNF on both synaptic markers were monitored in enteric nerve cell cultures and the presence of varicosities was determined by applying electron microscopy to the cultures.Human colonic specimens showed immunoreactivity for synaptophysin and synaptobrevin in both myenteric and submucosal ganglia as well as in nerve fibers. Both synaptic vesicle markers co-localized with the neuronal marker PGP 9.5 and exhibited granular accumulation patterns in the human and rat ENS. In cultured rat myenteric neurons GDNF treatment promoted expression of both synaptic vesicle markers and the formation of neuronal varicosities.The regulation of synaptophysin and synaptobrevin in enteric neurons by GDNF argues for the induction of functional neuronal networks in culture characterized by an increase of synaptogenesis. (C) 2013 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.