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+.
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