Gwag B J, Springer J E
Department of Neurology, Alzheimer Research Center, Hahnemann University School of Medicine, Philadelphia, PA 19102-1192.
Neuroreport. 1993 Nov 18;5(2):125-8. doi: 10.1097/00001756-199311180-00007.
In the present study, it is demonstrated that activation of NMDA receptors upregulates brain-derived neurotrophic factor (BDNF) in granule cells of the dentate gyrus and CA3 pyramidal neurons. BDNF mRNA levels in the granule cells peaked within 4 h, were still evident at 24 h, and returned to control levels within 48 h. In the CA3 region, BDNF mRNA levels were significantly increased at 2 h, peaked at 4 h, and returned to control values by 8 h following NMDA treatment. Finally, the effects of NMDA on BDNF mRNA expression were blocked by AP5, an NMDA receptor antagonist. These findings provide evidence that the in vivo activation of NMDA receptors may regulate the expression of this neurotrophin.
在本研究中，已证明N-甲基-D-天冬氨酸（NMDA）受体的激活可上调齿状回颗粒细胞和CA3锥体神经元中的脑源性神经营养因子（BDNF）。颗粒细胞中的BDNF mRNA水平在4小时内达到峰值，在24小时时仍很明显，并在48小时内恢复到对照水平。在CA3区域，NMDA处理后2小时BDNF mRNA水平显著升高，4小时达到峰值，并在8小时恢复到对照值。最后，NMDA受体拮抗剂AP5可阻断NMDA对BDNF mRNA表达的影响。这些发现提供了证据，表明NMDA受体的体内激活可能调节这种神经营养因子的表达。
