正构烷醇增强鱿鱼巨大轴突中的钠通道失活。
n-Alkanols potentiate sodium channel inactivation in squid giant axons.
作者信息
Oxford G S, Swenson R P
出版信息
Biophys J. 1979 Jun;26(3):585-90. doi: 10.1016/S0006-3495(79)85273-X.
Abstract
The effects of n-octanol and n-decanol on nerve membrane sodium channels were examined in internally perfused, voltage-clamped squid giant axons. Both n-octanol and n-decanol almost completely eliminated the residual sodium conductance at the end of 8-ms voltage steps. In contrast, peak sodium conductance was only partially reduced. This block of peak and residual sodium conductance was very reversible and seen with both internal and external alkanol application. The differential sensitivity of peak and residual conductance to alkanol treatment was eliminated after internal pronase treatment, suggesting that n-octanol and n-decanol enhance the normal inactivation mechanism rather than directly blocking channels in a time-dependent manner.
摘要
在内部灌注、电压钳制的枪乌贼巨大轴突中研究了正辛醇和正癸醇对神经膜钠通道的影响。在8毫秒电压阶跃结束时，正辛醇和正癸醇几乎完全消除了残余钠电导。相比之下，峰值钠电导仅部分降低。这种对峰值和残余钠电导的阻断是非常可逆的，并且在内部和外部应用链烷醇时都能观察到。在内部用链霉蛋白酶处理后，峰值和残余电导对链烷醇处理的差异敏感性消失，这表明正辛醇和正癸醇增强了正常的失活机制，而不是以时间依赖性方式直接阻断通道。
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