Wang S, Lees G J, Rosengren L E, Karlsson J E, Hamberger A, Haglid K G
Institute of Neurobiology, University of Göteborg, Sweden.
Neurochem Res. 1992 Oct;17(10):1005-9. doi: 10.1007/BF00966828.
An intrahippocampal injection of N-methyl-D-aspartate induced the appearance of degradation products of both the 68 kiloDalton neurofilament protein and the glial fibrillary acidic protein, as revealed by immunoblot techniques. The degradation of these two filament proteins was maximal at 10 days after the lesion. The degradation patterns were similar to those induced with calpains or calcium in vitro. There were no degradation effects on the 200 kD neurofilament protein as tested with both mono- and polyclonal antibodies. Consequently, the neuronal degeneration after excessive activation of NMDA receptors appears to involve calcium activation of proteolytic enzymes. The effects on the glial proteins are probably secondary to neuronal damage but could be related to calcium dependent processes.
通过免疫印迹技术发现，海马体内注射N-甲基-D-天冬氨酸会诱导68千道尔顿神经丝蛋白和胶质纤维酸性蛋白出现降解产物。这两种丝状蛋白的降解在损伤后10天达到最大程度。降解模式与体外使用钙蛋白酶或钙诱导的模式相似。使用单克隆和多克隆抗体检测时，对200 kD神经丝蛋白没有降解作用。因此，NMDA受体过度激活后的神经元变性似乎涉及蛋白水解酶的钙激活。对胶质蛋白的影响可能继发于神经元损伤，但可能与钙依赖性过程有关。
