The Lesioned Spinal Cord Is a “New” Spinal Cord: Evidence from Functional Changes after Spinal Injury in Lamprey

Treatments for spinal cord injury (SCI) have been categorized as those that rescue, reactivate, and rewire. Rewiring is the dominant approach in SCI research, and attempts to regenerate the connections damaged by the lesion. This is an obvious strategy given that SCI effects are caused by the loss of these inputs. This review summarizes published and unpublished work we have done on SCI in the lamprey, a lower vertebrate model system. The data suggests that even though locomotor behavior returns to pre-lesion levels, this reflects changes in spinal cord function and plasticity at all levels. Functional changes after SCI are demonstrated clinically by the appearance of spasticity once the period of spinal shock has passed. They have also been shown experimentally. All of these functional and structural changes will alter processing within spinal cord networks. This has led to the claim that the spinal cord below a lesion site is a “new” spinal cord

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  Synaptic inputs from individual regenerated axons also matched the properties in unlesioned animals, although this was associated with changes in release parameters.
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  Compensation instead seems to occur through diverse changes in cellular and synaptic properties in locomotor networks and proprioceptive systems below, but also above, the lesion site.
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  In regenerated axons below the lesion site N was generally reduced, consistent with the sparser anatomical connectivity; Pr was generally unchanged, consistent with a lack of difference in activity-dependent plasticity; but Q was consistently increased, suggesting a change in postsynaptic responsiveness.