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Biophys J, December 1999, p. 2999-3009, Vol. 77, No. 6

Effects of Channel Cytoplasmic Regions on the Activation Mechanisms of Cardiac versus Skeletal Muscle Na+ Channels

Eric S. Bennett

Department of Physiology and Biophysics, College of Medicine, University of South Florida, Tampa, Florida 33612 USA

Functional comparison of skeletal muscle (rSkM1) and cardiac (hH1) voltage-gated sodium channel isoforms expressed in Chinese hamster ovary cells showed rSkM1 half-activation (Va) and inactivation (Vi) voltages 7 and 10 mV more depolarized than hH1 Va and Vi, respectively. Internal papain perfusion removed fast inactivation from each isoform and caused a 20-mV hyperpolarizing shift in hH1 Va, with an insignificant change in rSkM1 Va. Activation voltage of the inactivation-deficient hH1 mutant, hH1Q3, was nearly identical to wild-type hH1 Va, both before and after papain treatment, with hH1Q3 Va also shifted by nearly 20 mV after internal papain perfusion. These data indicate that while papain removes both hH1 and rSkM1 inactivation, it has a second effect only on hH1 that causes a shift in activation voltage. Internal treatment with an antibody directed against the III-IV linker essentially mimicked papain treatment by removing some inactivation from each isoform and causing a 12-mV shift in hH1 Va, while rSkM1 Va remained constant. This suggests that some channel segment within, near, or interacting with the III-IV linker is involved in establishing hH1 activation voltage. Together the data show that rSkM1 and hH1 activation mechanisms are different and are the first to suggest a role for a cytoplasmic structure in the voltage-dependent activation of cardiac sodium channels.

Biophys J, December 1999, p. 2999-3009, Vol. 77, No. 6
© 1999 by the Biophysical Society   0006-3495/99/12/2999/11  $2.00


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