Cik M, Chazot P L, Stephenson F A
Department of Pharmaceutical Chemistry, School of Pharmacy, University of London, UK.
Eur J Pharmacol. 1994 Feb 15;266(3):R1-3. doi: 10.1016/0922-4106(94)90146-5.
Transient expression of wild-type N-methyl-D-aspartate, NMDAR1-1a/NMDAR2A heteromeric receptors, in mammalian cells yields cell death which was prevented by the inclusion of NMDA receptor antagonists in the cell culture media post-transfection. Transient expression of mutant NMDAR1-1a (N598Q)/NMDAR2A receptors resulted in a significant decrease in the percentage of cell death post-transfection. This mutation has been shown to reduce the Ca2+ permeability of cloned NMDA receptors. Thus these results provide indirect evidence for cell death via an NMDA receptor, Ca(2+)-mediated mechanism.
野生型N-甲基-D-天冬氨酸（N-methyl-D-aspartate，NMDAR1-1a/NMDAR2A）异聚体受体在哺乳动物细胞中的瞬时表达会导致细胞死亡，而在转染后于细胞培养基中加入NMDA受体拮抗剂可防止这种情况发生。突变型NMDAR1-1a（N598Q）/NMDAR2A受体的瞬时表达导致转染后细胞死亡百分比显著降低。已证明该突变可降低克隆的NMDA受体的Ca2+通透性。因此，这些结果为通过NMDA受体、Ca(2+)介导的机制导致细胞死亡提供了间接证据。
