n-Alkanols potentiate sodium channel inactivation in squid giant axons.
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.
D020003:1-Octanol; D000818:Animals; D001369:Axons / Q000502:physiology*; D049832:Decapodiformes; D004553:Electric Conductivity; D005233:Fatty Alcohols / Q000494:pharmacology*; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology*; D000442:Octanols / Q000494:pharmacology*; D012964:Sodium / Q000378:metabolism*
D005233:Fatty Alcohols; D007473:Ion Channels; D000442:Octanols; C029383:n-decyl alcohol; D012964:Sodium; D020003:1-Octanol