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首页> 美国卫生研究院文献>The Journal of Physiology >Inhibition of oxidative metabolism increases persistent sodium current in rat CA1 hippocampal neurons
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Inhibition of oxidative metabolism increases persistent sodium current in rat CA1 hippocampal neurons

机译：氧化代谢的抑制作用增加大鼠CA1海马神经元的持续钠电流

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class="enumerated" style="list-style-type:decimal">Whole-cell patch-clamp recordings from freshly dissociated rat CA1 neurons revealed a large transient Na+ current (INa,T) and a smaller, inactivation-resistant persistent Na+ current (INa,P). Both currents could be blocked with TTX.The average current densities of INa,T and INa,P in thirty cells were 111.0 ± 9.62 and 0.87 ± 0.13 pA pF−1, respectively.Inhibiting oxidative phosphorylation by adding 5 mm sodium cyanide to the pipette solution significantly increased the amplitude of INa,P but had no significant effect on the amplitude of INa,T.Exposing CA1 neurons to hypoxia for more than 7 min caused an increase in the amplitude of INa,P. There was also a delayed decrease in the amplitude of INa,T.INa,P was more sensitive to the Na+ channel blockers TTX and lidocaine than INa,T. The IC50 for the effect of TTX on INa,P was 9.1 ± 1.2 nM whereas the IC50 for INa,T was 37.1 ± 1.2 nM, approximately 4-fold higher. Lidocaine (lignocaine; 1 μm) reduced INa,P to 0.24 ± 0.15 of control (n = 4) whereas INa,T was essentially unaffected (0.99 ± 0.11, n = 4).These results show that INa,P is increased when oxidative metabolism is blocked in CA1 neurons. The persistent influx of Na+ through non-inactivating Na+ channels can be blocked by concentrations of Na+ channel blockers that do not affect INa,T.
机译：class =“ enumerated” style =“ list-style-type：decimal”> <！-list-behavior =枚举前缀-word = mark-type = decimal max-label-size = 0-> 新鲜分离的大鼠CA1神经元的全细胞膜片钳记录显示了一个大的瞬时Na + 电流（INa，T）和一个较小的，耐失活的持久性Na + 电流（INa，P）。 三十个电池中INa，T和INa，P的平均电流密度分别为111.0±9.62和0.87±0.13 pA pF -1 ， 分别在移液管中加入5 mm氰化钠抑制氧化磷酸化，显着增加了INa，P的幅度，但对INa，T的幅度没有显着影响。 将CA1神经元暴露于缺氧状态超过7分钟会导致INa，P振幅增加。 INa，P比Naa，T对Na + 通道阻滞剂TTX和利多卡因更敏感。 TTX对INa，P的作用的IC50为9.1±1.2 nM，而INa，T的IC50为37.1±1.2 nM，大约高4倍。利多卡因（利多卡因； 1μm）可将INa，P降至对照组（n = 4）的0.24±0.15，而INa，T基本不受影响（0.99±0.11，n = 4）。 这些结果表明，当CA1神经元的氧化代谢受阻时， I Na，P 增加。 Na + 通道通过非灭活的Na + 通道的持久流入可以通过不影响 + 通道阻滞剂的浓度来阻止> I Na，T 。

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