Small D L, Poulter M O, Buchan A M, Morley P
Institute for Biological Sciences, National Research Council of Canada, Ottawa, Ontario.
Neurosci Lett. 1997 Aug 29;232(2):87-90. doi: 10.1016/s0304-3940(97)00592-2.
Brain insults, including cerebral ischemia, can alter glutamate receptor subunit expression in vulnerable neurons. Understanding these post-ischemic changes in glutamate receptors could enhance our ability to identify specific, novel neuroprotective compounds. Reverse transcription-polymerase chain reaction (RT-PCR) amplification was used to quantify the altered expression of the N-methyl-D-aspartate (NMDA) NR2A, NR2B and NR2C subunits relative to one another in rat hippocampal slices in resistant and vulnerable regions following in vitro oxygen-glucose deprivation. Ninety minutes after re-oxygenation and return to 10 mM glucose, there was a significant increase in the expression of NR2C relative to NR2B and NR2A in the slice as a whole, as well as in the selectively vulnerable CA1 region and the resistant CA3 and dentate gyrus regions.
脑部损伤,包括脑缺血,可改变易损神经元中谷氨酸受体亚基的表达。了解谷氨酸受体的这些缺血后变化,可能会增强我们识别特定新型神经保护化合物的能力。采用逆转录-聚合酶链反应(RT-PCR)扩增法,对体外氧糖剥夺后大鼠海马切片中抗性和易损区域的N-甲基-D-天冬氨酸(NMDA)NR2A、NR2B和NR2C亚基相对彼此的表达变化进行定量。复氧并恢复至10 mM葡萄糖90分钟后,相对于NR2B和NR2A,切片整体、选择性易损的CA1区以及抗性的CA3区和齿状回区中NR2C的表达显著增加。