Yamaguchi K, Yamaguchi F, Miyamoto O, Hatase O, Tokuda M
Department of Physiology, Faculty of Medicine, Kagawa Medical University, Japan.
J Cereb Blood Flow Metab. 1999 Apr;19(4):370-5. doi: 10.1097/00004647-199904000-00002.
The ischemic tolerance is known to show protective effects on the neurons and the restricted Ca2+ influx through Ca2+ channels might be involved. In alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor, ribonucleic acid (RNA) editing of the GluR2 subunit determines receptor desensitization and Ca2+ permeability. The authors investigated the effect of ischemic tolerance on the messenger RNA editing of Q/R and R/G sites of GluR2 subunit in hippocampus. It was found that the rate of RNA editing in Q/R site showed no change (100% edited), whereas that in R/G site decreased significantly (83.3% normal editing level to 60.4%) at day 3 (preconditioning period) and returned to normal level at day 14 (after preconditioning period). Further investigation revealed that the decrease of editing rate in ischemic tolerance resulted mainly from the decrease of editing in CA1 area.
已知缺血耐受对神经元具有保护作用，这可能与通过钙离子通道限制钙离子内流有关。在α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）受体中，谷氨酸受体2（GluR2）亚基的核糖核酸（RNA）编辑决定了受体的脱敏作用和钙离子通透性。作者研究了缺血耐受对海马体中GluR2亚基Q/R和R/G位点信使核糖核酸编辑的影响。结果发现，Q/R位点的RNA编辑率没有变化（100%编辑），而在第3天（预处理期），R/G位点的RNA编辑率显著下降（从正常编辑水平的83.3%降至60.4%），并在第14天（预处理期后）恢复到正常水平。进一步研究表明，缺血耐受时编辑率的下降主要是由于CA1区编辑的减少。
