McDonald J W, Levine J M, Qu Y
Center for the Study of Nervous System Injury and Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA.
Neuroreport. 1998 Aug 24;9(12):2757-62. doi: 10.1097/00001756-199808240-00014.
We have recently shown that galactocerebroside (Gal-C)-expressing oligodendrocytes are highly vulnerable to (AMPA)/kainate receptor-mediated death. Here we examined the vulnerability of cells at different developmental stages of the oligodendrocyte lineage to AMPA/kainate receptor-mediated excitotoxicity. Oligodendrocyte precursor cells, pre-oligodendrocytes and mature oligodendrocytes were killed by 24 h exposures to low concentrations of kainate (30-100 microM). Death was attenuated by the AMPA/kainate receptor antagonist 6-nitro-7-sulfamoylbenzo(f)quinoxaline-2,3-dione (NBQX). The high vulnerability of oligodendrocytes and their precursors to AMPA/kainate receptor excitotoxicity may represent an important mechanism of white matter damage resulting from trauma or ischemia in the perinatal and adult central nervous system (CNS).
我们最近发现,表达半乳糖脑苷脂(Gal-C)的少突胶质细胞极易受到α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)/海人酸受体介导的死亡影响。在此,我们研究了少突胶质细胞谱系不同发育阶段的细胞对AMPA/海人酸受体介导的兴奋性毒性的易感性。少突胶质前体细胞、前少突胶质细胞和成熟少突胶质细胞在暴露于低浓度海人酸(30 - 100微摩尔)24小时后死亡。AMPA/海人酸受体拮抗剂6-硝基-7-氨磺酰基苯并[f]喹喔啉-2,3-二酮(NBQX)可减轻细胞死亡。少突胶质细胞及其前体细胞对AMPA/海人酸受体兴奋性毒性的高度易感性可能是围产期和成人中枢神经系统(CNS)创伤或缺血导致白质损伤的重要机制。