Abstract
We found previously that the external surface of frog skeletal muscle fibers can be irreversibly modified by treatment with the amino group-specific reagent, trinitrobenzene sulfonic acid (TNBS). Reaction of the muscle membrane with TNBS permanently shifts the potential dependence of the sodium channel inactivation gating process, h infinity, to more hyperpolarized potentials. The experiments presented here show nearly identical effects on the sodium currents of voltage-clamped frog node of Ranvier in the presence of TNBS. In contrast to the results in muscle, in myelinated nerve the voltage dependence of sodium-channel inactivation returns rapidly to control values following a brief exposure to TNBS. We have used partial demyelination to test the hypothesis that recovery of the normal voltage dependence for h infinity following TNBS treatment is due to lateral diffusion of reacted groups away from the sodium channels in the node. We find that increasing the membrane area exposed to TNBS by partial demyelination greatly slows reversal of the TNBS effects. This result suggests that a modifiable membrane component that affects sodium channel gating is mobile in the plane of the membrane and can rapidly diffuse between nodal and internodal regions.