Ishiuchi S, Tsuzuki K, Yamada N, Okado H, Miwa A, Kuromi H, Yokoo H, Nakazato Y, Sasaki T, Ozawa S
Department of Neurosurgery, Gunma University School of Medicine, Maebashi, Japan.
Neuroreport. 2001 Mar 26;12(4):745-8. doi: 10.1097/00001756-200103260-00026.
AMPA type-glutamate receptor channels (AMPARs) assembled without the GluR2 (GluR-B) subunit are characterized by high Ca2+ permeability, and are expressed abundantly in cerebellar Bergmann glial cells. Here we show that the morphology of cultured Bergmann glia-like fusiform cells derived from the rat cerebellum was changed by manipulating expression of Ca2+-permeable AMPARs using adenoviral vector-mediated gene transfer. Converting endogenous Ca2+-permeable AMPARs into Ca2+-impermeable channels by viral-mediated transfer of GluR2 gene induced retraction of glial processes. In contrast, overexpression of Ca2+-permeable AMPARs markedly elongated glial processes. The process extension was blocked by 2,3-Dihydroxy-6-nitro-7-sulfamoylbenzo(F)quinoxaline (NBQX), a specific antagonist of AMPAR. These results indicate that glutamate regulates the morphology of glial processes by activating Ca2+-permeable AMPARs.
不含GluR2（GluR - B）亚基组装而成的α - 氨基 - 3 - 羟基 - 5 - 甲基 - 4 - 异恶唑丙酸（AMPA）型谷氨酸受体通道具有高钙离子通透性的特点，并且在小脑伯格曼胶质细胞中大量表达。在此我们表明，通过腺病毒载体介导的基因转移来操控钙离子通透型AMPA受体的表达，源自大鼠小脑的培养的类伯格曼胶质细胞样梭形细胞的形态会发生改变。通过病毒介导的GluR2基因转移将内源性钙离子通透型AMPA受体转变为钙离子不通透通道会诱导胶质细胞突起回缩。相反，钙离子通透型AMPA受体的过表达显著延长了胶质细胞突起。突起的延长被AMPA受体的特异性拮抗剂2,3 - 二羟基 - 6 - 硝基 - 7 - 氨磺酰基苯并（F）喹喔啉（NBQX）所阻断。这些结果表明，谷氨酸通过激活钙离子通透型AMPA受体来调节胶质细胞突起的形态。
