Abstract
The specific permeability properties of isolated rat fibers with diphtheria toxin induced paranodal demyelination were investigated in potential clamp experiments. Nodal widening (4-6 .mu.m) and paradnodal demyelination (20-90 .mu.m) were associated with a very large increase in the normally low delayed K-permeability (< 10 times). The resting K-permeability (which was comparatively large in the rat fibers) was similarly increased, which decreased action potential amplitude and excitability. Fibers with paranodal demyelination had, in addition, a large increase in the maximum peak Na-permeability (2-5 times the normal), which indicated that excitability was upheld by formation of new Na-permeability sites. The conduction defects in demyelinated fibers can therefore not be related to the size of the demyelination, but to the specific permeability changes in the demyelinated segment.