NORMAL-ALKANOLS POTENTIATE SODIUM-CHANNEL INACTIVATION IN SQUID GIANT-AXONS

被引:50
作者
OXFORD, GS [1 ]
SWENSON, RP [1 ]
机构
[1] DUKE UNIV,MED CTR,DEPT PHYSIOL & PHARMACOL,DURHAM,NC 27710
基金
美国国家科学基金会;
关键词
D O I
10.1016/S0006-3495(79)85273-X
中图分类号
Q6 [生物物理学];
学科分类号
071011 ;
摘要
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. © 1979, The Biophysical Society. All rights reserved.
引用
收藏
页码:585 / 590
页数:6
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