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In the spinal cord of the lamprey, regeneration of giant reticulospinal axons occurs following transection. We show that partial degeneration of the proximal axonal segment, or “die-back,” also occurs following spinal transection and it precedes regenerative outgrowth. The die-back during the first 5 days post-transection is reduced significantly by application of a 10-microA DC current across the site of transection, with the cathode distal to the lesion. Reversing the polarity of the applied current (cathode proximal to the lesion) increases the extent of axonal die-back relative to the sham-treated controls. Following spinal transection, saline-filled wick electrodes were implanted in the body musculature on either side of the lesion. Electrically treated animals received current across the lesion for 5 days, while the sham- treated controls received no current. After 5 days, several giant axons in each preparation were injected intracellularly in the spinal cord with the dye Lucifer Yellow. The extent of axonal die-back in the proximal cord stump was determined in the filled fibers by measuring the distance of the axon end from the site of lesion. The mean distances of axonal die-back were as follows: controls, 1750 microns +/- 45 SEM; cathode-distal, 740 microns +/- 33 SEM; cathode-proximal, 2820 microns +/- 60 SEM. These differences between the treatment groups proved to be significant using the Wilcoxon rank sum test. We propose that die-back is caused by the entry of cations driven into the cut surface of the cord by the endogenous injury current. The applied DC current interacts with the endogenous current of injury to either decrease or increase the flow of cations into the cord, depending on the direction of applied current flow across the lesion. This in turn causes a corresponding reduction or enhancement of the axonal die-back.

Modification of retrograde degeneration in transected spinal axons of the lamprey by applied DC current