Neural tissue transplants in immature spinal cord injury models promote anatomical plasticity involving both late-developing and regenerating neurons, which may underlie functional recovery.
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Supports mechanistic insights into transplant-mediated recovery in immature models; leaves open translation to adult human spinal cord injury.
We are using neural tissue transplantation after spinal cord injury to identify the rules which determine the response of young neurons to injury, to identify the mechanisms underlying anatomical plasticity and recovery of function following spinal cord injury, and to determine the conditions which change during development, leading to the more restricted growth capacity of mature neurons following injury. Spinal cord lesions at birth interrupt different pathways at different relative stages in their development. Neural tissue transplants modify the response of the immature central nervous system neurons to injury. In the current studies, we have used neuroanatomical and behavioral methods to compare the response of the late-developing corticospinal pathway with that of brainstem-spinal pathways which are intermediate in their development and that of the relatively mature dorsal root pathway. We find that both late-developing and regenerating neuronal populations contribute to the transplant-induced anatomical plasticity, and suggest that this anatomical plasticity underlies the transplant-mediated sparing and recovery of function.
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Bregman et al. (1991) studied this question.
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