Alsbo C W, Wrang M L, Johansen F F, Diemer N H
Laboratory of Neuropathology, Institute of Molecular Pathology, University of Copenhagen, Denmark.
Neuroreport. 2000 Feb 7;11(2):311-5. doi: 10.1097/00001756-200002070-00018.
Quantitative PCR was used to analyse the expression of GluR1, GluR2, GluR2 flip, GluR2 flop and GluR3 mRNA in animals after ischemia and tolerance-inducing ischemia. The ischemic animals showed a decrease in the GluRs to approximately 30%, except for GluR2-flip, which decreased to 75%. The tolerance animals displayed regulation of GluR1 to 75%, GluR2 and GluR2-flop to 283% and 265% respectively. We did not find a correlation between GluR2 regulation and cell loss in the ischemic group. The selective upregulation of GluR2/GluR2 flop in tolerant animals indicates a possible mechanism for enhanced AMPA receptor desensitisation leading to tolerance to ischemia.
采用定量聚合酶链反应(Quantitative PCR)分析缺血及诱导耐受缺血后动物体内谷氨酸受体1(GluR1)、谷氨酸受体2(GluR2)、GluR2翻转异构体(GluR2 flip)、GluR2摆动异构体(GluR2 flop)和谷氨酸受体3(GluR3)信使核糖核酸(mRNA)的表达情况。除GluR2翻转异构体降至75%外,缺血动物体内谷氨酸受体(GluRs)降至约30%。耐受动物体内,GluR1上调至75%,GluR2和GluR2摆动异构体分别上调至283%和265%。我们未发现缺血组中GluR2调节与细胞丢失之间存在相关性。耐受动物体内GluR2/GluR2摆动异构体的选择性上调表明,增强α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)受体脱敏从而导致对缺血耐受的一种可能机制。