Abstract— —We have compared retrograde axonal transport of 3H‐labeled protein in normal rat motor and sensory axons, and axons which were injured by a distal ligation of the sciatic nerve. After injection of L‐[3H]leucine into the vicinity of the neuron cell bodies, labeled protein was transported into the axons. A premature return of protein towards the cell bodies occurred in the injured axons, which we interpret as a reversal of axonal transport occurring at the site of injury. We estimate that reversal of transport occurred within 1.9–2.4 h of the arrival of labeled protein at the injury, and that the minimum velocity of the subsequent retrograde transport was 112–133 mm day−1. The ability of the injured axons to reverse transport developed about 0.8 h after making the injury. A large fraction of the orthograde transported protein was returned towards the cell body: it is estimated that by 28 h after labeled protein in sensory axons reached the injury, 46% of the3H‐labeled protein originally transported to the injury site had been returned. In intact sensory nerves at this time only 15% of the transported protein had returned. It is suggested that axonal injury produces a sudden increase in the return of newly synthesized protein to the cell body, and that this might serve as a signal for chromatolysis.

Abstract— Orthograde and retrograde axonal transport were studied in rat sciatic nerves which had been crushed and either allowed to regenerate, or prevented from doing so by tightly ligaturing the nerve. At various intervals after crushing the nerve. L‐[3H]leucine was injected into the lumbosacral spinal cord. and the subsequent transport of labeled protein in motoneuron axons was quantitated by measuring the accumulation of labeled protein at collection crushes made proximal to the original nerve crush. Accumulations proximal to the collection crushes (orthograde transport) 9‐11 h after injection (p.i.). decreased within I day of nerve injury, but returned to normal values as regeneration proceeded. In non‐regenerating nerves accumulations remained depressed for at least 30 days. Accumulations distal to the collection crushes (retrograde transport) 9‐11 h pi. increased over the first 5 days following injury but returned to normal values as regeneration proceeded. In non‐regenerating nerves accumulations remained elevated. The time‐course of retrograde transport of newly‐synthesized protein also returned to normal during nerve regeneration. It is suggested that changes in retrograde transport during regeneration may inform the neuron cell body of the progress of regeneration and elicit appropriate metabolic responses. among which may be the changes in orthograde transport that follow axotomy.

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