Spatiotemporal gradients of intra‐axonal [Na+] after transection and resealing in lizard peripheral myelinated axons.

1. Post‐transection changes in intracellular Na+ ([Na+]i) were measured in lizard peripheral axons ionophoretically injected with the Na(+)‐sensitive ratiometric dye, sodium‐binding benzofuran isophthalate (SBFI). 2. Following axonal transection in physiological saline [Na+]i increased to more than 100 mM in a region that quickly extended hundreds of micrometers from the transection site. This post‐transection increase in [Na+]i was similar when the bath contained 5 microM tetrodotoxin, but was absent in Na(+)‐free solution. Depolarization of uncut axons in 50 mM K+ produced little or no elevation of [Na+]i until veratridine was added. These results suggest that the post‐transection increase in [Na+]i was due mainly to Na+ entry via the cut end, rather than via depolarization‐activated Na+ channels. 3. The spatiotemporal profile of the post‐transection increase in [Na+]i could be accounted for by movement of Na+ from the cut end with an apparent diffusion coefficient of 1.3 x 10(‐5) cm2 s‐1. 4. [Na+]i began to decline toward resting levels by 20 +/‐ 15 min (mean +/‐ S.D.) post‐transection, except in regions of the axon within 160 +/‐ 85 microns of the transection site, where [Na+]i remained high. The boundary between axonal regions in which [Na+]i did or did not recover probably defines a locus of resealing of the axonal membrane. 5. [Na+]i returned to resting values within about 1 h after resealing, even in axonal regions where the normal transmembrane [Na+] gradient had completely dissipated. The recovery of [Na+]i was faster and reached lower levels than expected by diffusional redistribution of Na+ along the axon. Partial recovery occurred even in an isolated internode, indicating that the internodal axolemma can actively extrude Na+.