Small D L, Murray C L, Mealing G A, Poulter M O, Buchan A M, Morley P
Cellular Neurobiology Group, Institute for Biological Sciences, National Research Council of Canada, Ottawa, Ontario.
Neurosci Lett. 1998 Aug 21;252(3):211-4. doi: 10.1016/s0304-3940(98)00587-4.
N-methyl-D-aspartate (NMDA) receptor subunit expression changes during development and following injury in several brain regions. These changes may be mediated by neurotrophic factors, such as brain derived neurotrophic factor (BDNF). Exposure of cultured cortical neurons to BDNF (100 ng/ml) for 24 h produced a significant decrease in the NMDA-induced whole-cell currents sensitive to the NR2B subunit selective NMDA receptor antagonist, CP-101,606, suggesting a relative decrease in NR2B subunit expression. There was a significant increase in NR2A by Western blot analysis. Consistent with the electrophysiology and Western blot analysis, reverse transcriptase-polymerase chain reaction (RT-PCR) amplification revealed that BDNF caused a significant increase in relative NR2A subunit expression, a significant decrease in relative NR2B subunit expression and no change in relative NR2C subunit expression. These results suggest that BDNF enhances NMDA receptor maturation, warranting further study of the mechanism of BDNF effects on NMDA receptor subunit expression and the role these effects play in development and neuronal injury.
N-甲基-D-天冬氨酸(NMDA)受体亚基的表达在多个脑区的发育过程及损伤后会发生变化。这些变化可能由神经营养因子介导,如脑源性神经营养因子(BDNF)。将培养的皮质神经元暴露于BDNF(100 ng/ml)24小时后,对NR2B亚基选择性NMDA受体拮抗剂CP-101,606敏感的NMDA诱导的全细胞电流显著降低,这表明NR2B亚基的表达相对减少。通过蛋白质印迹分析发现NR2A显著增加。与电生理学和蛋白质印迹分析结果一致,逆转录聚合酶链反应(RT-PCR)扩增显示,BDNF导致NR2A亚基相对表达显著增加,NR2B亚基相对表达显著降低,而NR2C亚基相对表达无变化。这些结果表明,BDNF可促进NMDA受体成熟,这值得进一步研究BDNF对NMDA受体亚基表达的作用机制以及这些作用在发育和神经元损伤中所起的作用。