Sodium and potassium channels in demyelinated and remyelinated mammalian nerve

Abstract

Demyelination of peripheral axons initially causes failure of action potential conduction, probably because the internodal membrane lacks sodium channels^1,2. However, Bostock and Sears³ showed that 3–14 days after demyelination of rat nerve with diphtheria toxin, some axons develop regenerative inward currents in the internodal membrane permitting continuous (non-saltatory) conduction. In nerves that have remyelinated or regenerated, the number of nodes per unit length of fibre characteristically increases greatly^4,5. As the internodal membrane does not normally possess sodium channels^1,2, both the earlier appearance of continuous conduction in the demyelinated nerve and the later presence of extra nodes in the remyelinated nerve require either a laying down of new sodium channels or a redistribution of the sodium channels in the original nodes. The present experiments examine the changes in the total number of sodium channels, measured by saxitoxin-binding capacity¹, that occur in rabbit sciatic nerves which have been demyelinated in vivo with lysolecithin^2,5 and then allowed to remyelinate. The results provide no evidence for the formation of new sodium channels during the early stage, when continuous conduction may develop, but show clearly that new channels are formed during remyelination.