Mouse sciatic nerves from the degeneration-resistant strain C57BL/6/Wld (Ola) were surgically injected with lysolecithin to induce focal demyelination. Three days later they were transected adjacent to the spinal cord to eliminate contact of the axons with their cell bodies. The Na+ channel distribution was assessed by immunocytochemistry and followed at several stages of remyelination. Control experiments were performed on nerves that were injected but not cut. At (3 + 4) days, namely, nerves cut 3 days post-injection and examined 4 days after cutting, axons contained fully demyelinated regions. Na+ channel clusters appeared only at heminodes and at isolated sites that are likely to represent original nodes of Ranvier. During the next few days proliferating Schwann cells adhered to the axons and extended their processes. Clusters of Na+ channels appeared at their edges, and as the Schwann cells elongated the distance between these aggregates increased. A few clusters associated with neighboring Schwann cells approached each other and appeared to coalesce at sites where presumably new nodes of Ranvier would be formed. Beyond (3 + 6) days excessive degeneration of the transected axons precluded further observations. In the uncut controls, the spatio-temporal sequence of Schwann cell proliferation and channel patch formation and movement was similar to that described above, although myelin formation was somewhat faster than in the cut axons. It is concluded that Na+ channel aggregation associated with the early stages of remyelination is not dependent upon continuous communication of the axon with its cell body and is under local control.