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 micrometres from the transection site. This post-transection increase in [Na⁺](i) was similar when the bath contained 5 μM 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 μm 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⁺.