Aitken P G, Balestrino M, Somjen G G
Department of Physiology, Duke University Medical Center, Durham, NC 27710.
Neurosci Lett. 1988 Jun 29;89(2):187-92. doi: 10.1016/0304-3940(88)90379-5.
Rat hippocampal slices were exposed to a hypoxic insult in control medium or while exposed to the N-methyl-D-aspartate (NMDA) receptor antagonists DL-2-amino-7-phosphonoheptanoic acid (100 microM) or DL-2-amino-5-phosphonovaleric acid (25 or 100 microM). Synaptic transmission between Schaffer collaterals and CA 1 pyramidal cells was evaluated before and after the hypoxic period, and the DC potential in the CA 1 pyramidal cell layer was monitored during the hypoxic period. Neither antagonist significantly increased the proportion of slices in which synaptic transmission recovered following hypoxia, nor did they increase the latency of the spreading depression-like anoxic depolarization. We suggest that NMDA receptors are not involved in neural damage caused by severe hypoxia with sudden onset, while they may play a role in the effects of more moderate, gradual onset hypoxia and in post-ischemic reperfusion effects.
将大鼠海马切片置于对照培养基中，或在暴露于N-甲基-D-天冬氨酸（NMDA）受体拮抗剂DL-2-氨基-7-磷酸庚酸（100微摩尔）或DL-2-氨基-5-磷酸戊酸（25或100微摩尔）的情况下进行低氧损伤。在低氧期前后评估Schaffer侧支与CA1锥体细胞之间的突触传递，并在低氧期监测CA1锥体细胞层的直流电位。两种拮抗剂均未显著增加低氧后突触传递恢复的切片比例，也未增加类扩散性抑制性缺氧去极化的潜伏期。我们认为，NMDA受体不参与由突然发作的严重低氧引起的神经损伤，而它们可能在更中度、逐渐发作的低氧效应以及缺血后再灌注效应中起作用。
