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Cell Death And Changes In The Retrograde Transport Of Horseradish Peroxidase In Rubrospinal Neurons Following Spinal Cord Hemisection In The Adult Rat
H. Goshgarian, J. Koistinen, E. R. Schmidt
Published 1983 · Biology, Medicine
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Most of the hypotheses that have been proposed to explain why the injured mammalian spinal cord is not capable of extensive regeneration have suggested that the internal milieu of the injured spinal cord is not conducive to repair. Relatively little attention has been directed toward neuronal cell death as being contributory to the minimal amount of spinal cord regeneration. The present study suggests that the availability of regenerating axons in the injured spinal cord may be limited by the death of axotomized supraspinal neurons in the adult mammal. Adult rats were subjected to a right spinal cord hemisection at T1 followed by a second, more rostral right hemisection at C2 Horseradish peroxidase (HRP) was injected into the rostral hemisection site to acquire information on the metabolic changes that occur in HRP‐labeled rubrospinal neurons after axotomy. In the experimental animals, a delay of 9‐219 days occurred between the two operations whereas there was no delay between the two procedures in the control animals. An analysis of neuronal counts indicated that although there was a statistically significant (P < 0.01) decrease in the number of labeled rubrospinal neurons in the contralateral red nucleus of the experimental animals compared to controls, there was also a smaller, yet significant (P < 0.01) increase in the number of nonlabeled neurons in the experimental animals. The mean total number (both labeled and nonla beled) of neurons in the experimental animals (2,269 ± 348 cells), however, was significantly lower (P < 0.01) than the mean total number of neurons in the control animals (3,473 ± 488 cells). Thus, it is concluded that extensive cell death occurs in the red nucleus of the adult rat following spinal cord hemisection.
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