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  • By Author: Tator, Charles H. x
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Charles H. Tator, Alex S. Rivlin, Anthony J. Lewis and Beatrice Schmoll

✓ The concentration of axons in the pyramidal tract of normal and spinal cord-injured rats was determined by counting axons in sections of spinal cord stained by the Holmes technique. In the normal rat the axon concentration was uniform in the cervical, thoracic, and lumbar regions, although the size of the tract diminished progressively with its descent in the cord. After acute cord transection or compression injury, the axon concentration distal to the injury site diminished markedly. However, an appreciable number of distal axons persisted after injury, due to either delayed degeneration or to the presence of an admixture of afferent fibers. The axonal counting technique developed in this study should be helpful in experiments on spinal cord injury and regeneration.

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Charles H. Tator, Alex S. Rivlin, Anthony J. Lewis and Beatrice Schmoll

✓ Studies were performed on the effect of triiodo-L-thyronine (T3) on clinical recovery and axonal counts in the pyramidal tract of 56 rats subjected to an acute spinal cord compression injury at T-7. The T3 was given at a daily dose of 5 µg/kg for 4 weeks to 28 rats in the treatment group. The treatment and control animals were tested weekly for clinical recovery, and cord function as determined by the inclined-plane technique. Groups of animals were killed at 4 weeks and 12 weeks, and the axons in the pyramidal tract cephalad and caudad to the injury site were counted in sections prepared with Holmes' silver stain.

There was no difference in clinical recovery between the treatment and control groups. This negative result contrasts with other studies which showed improved recovery of cord-injured animals treated with thyroid hormones. The possible explanations for this discrepancy are discussed. Similarly, there was no difference in the axon counts between the treated and control groups. Thus, T3 did not improve recovery or axonal regeneration in the pyramidal tract of rats after acute spinal cord compression injury. Between 4 and 12 weeks, there was a marked reduction in the cephalad axon counts in the pyramidal tract in both groups, indicating that approximately 50% of the axons in the pyramidal tract had undergone retrograde degeneration or dying back by 12 weeks after this degree of injury. The T3 did not affect the degree of retrograde degeneration.