Hill R H, Brodin L, Grillner S
Nobel Institute for Neurophysiology, Karolinska Institutet, Stockholm, Sweden.
Brain Res. 1989 Oct 16;499(2):388-92. doi: 10.1016/0006-8993(89)90790-7.
Current- and voltage-clamp techniques were used to analyze the mechanisms underlying the repolarization during N-methyl-D-aspartate (NMDA)-induced, tetrodotoxin-resistant pacemaker-like oscillations in lamprey spinal neurons. Long-lasting depolarizing current pulses (15-40 mV, 50-400 ms, tetrodotoxin and tetraethylammonium present) were followed by hyperpolarizing afterpotentials even when NMDA receptors were blocked, but they were markedly enhanced by application of N-methyl-D,L-aspartate (NM(DL)A). The afterpotentials were depressed by replacing Ca2+ with Ba2+. During voltage-clamp NM(DL)A enhanced a Ba2+-sensitive outward tail current following voltage steps of 15-40 mV. The outward current remained after injection of Cl-, as did the NMDA-induced membrane potential oscillations observed under current-clamp. These results suggest that the repolarization during NMDA-induced oscillations is due to Ca2+ entry both via NMDA-gated channels and conventional voltage-gated Ca2+ channels, leading to an activation of Ca2+-dependent K+ channels. The afterhyperpolarization following single action potentials, which is also due to Ca2+-dependent K+ channels, was not significantly altered by NMDA receptor activation, suggesting a different location of the Ca2+ entry during the two conditions in relation to the location of the activated Ca2+-dependent K+ channels.
采用电流钳和电压钳技术，分析七鳃鳗脊髓神经元中N-甲基-D-天冬氨酸（NMDA）诱导的、河豚毒素抗性起搏器样振荡期间复极化的潜在机制。即使NMDA受体被阻断，在施加持久去极化电流脉冲（15 - 40 mV，50 - 400 ms，存在河豚毒素和四乙铵）后仍会出现超极化后电位，但应用N-甲基-D，L-天冬氨酸（NM（DL）A）可使其显著增强。用Ba²⁺替代Ca²⁺后，后电位降低。在电压钳实验中，NM（DL）A增强了15 - 40 mV电压阶跃后的Ba²⁺敏感外向尾电流。注入Cl⁻后外向电流依然存在，电流钳下观察到的NMDA诱导的膜电位振荡也是如此。这些结果表明，NMDA诱导振荡期间的复极化是由于Ca²⁺通过NMDA门控通道和传统电压门控Ca²⁺通道进入，导致Ca²⁺依赖性K⁺通道激活。单动作电位后的超极化后电位同样归因于Ca²⁺依赖性K⁺通道，NMDA受体激活并未使其发生显著改变，这表明在这两种情况下Ca²⁺进入的位置与激活的Ca²⁺依赖性K⁺通道的位置不同。
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