Lovinger D M, Weight F F
Section of Electrophysiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20852.
Neurosci Lett. 1988 Dec 5;94(3):314-20. doi: 10.1016/0304-3940(88)90037-7.
The effects of glutamate, glutamate receptor agonists and substances that affect glutamate responses were studied, using the whole-cell patch-clamp technique, on neurons isolated from adult rat dorsal root ganglia. In current-clamp, glutamate (100 microM) or the excitatory amino acid receptor agonist N-methyl-D-aspartate (NMDA; 10 or 100 microM) induced membrane depolarization. Under voltage-clamp, these compounds induced an inward current that was voltage-dependent in the presence of Mg2+. The NMDA-induced current was inhibited by the NMDA receptor antagonist D,L-2-amino-5-phosphono-valerate (APV; 100 microM), and potentiated by 100 nM glycine. Few neurons responded to the receptor agonists kainate (100 microM), or quisqualate (1-10 microM). These observations suggest that glutamate-induced depolarization of primary sensory neurons is mediated predominantly by NMDA receptors.
利用全细胞膜片钳技术，研究了谷氨酸、谷氨酸受体激动剂以及影响谷氨酸反应的物质对从成年大鼠背根神经节分离出的神经元的作用。在电流钳模式下，谷氨酸（100微摩尔）或兴奋性氨基酸受体激动剂N-甲基-D-天冬氨酸（NMDA；10或100微摩尔）可诱导膜去极化。在电压钳模式下，这些化合物在Mg2+存在时诱导出一种电压依赖性的内向电流。NMDA诱导的电流被NMDA受体拮抗剂D，L-2-氨基-5-磷酸戊酸（APV；100微摩尔）抑制，并被100纳摩尔甘氨酸增强。很少有神经元对受体激动剂海人藻酸（100微摩尔）或quisqualate（1 - 10微摩尔）有反应。这些观察结果表明，谷氨酸诱导的初级感觉神经元去极化主要由NMDA受体介导。
