Abstract
In the Bunge repair strategy, a tube containing a Schwann cell cable bridges the cord lesion. Regenerating axons penetrate the proximal cord-graft interface and grow through the Schwann cell cable but the axons do not grow across distal cord-graft interface and into distal cord stump. Regeneration of axons can be promoted by applying neurotrophic factors in graft. Adding a matrix containing genes encoding for neurotrophic factors in the SC bridge between the proximal and distal cord-graft interfaces may promote axonal regeneration into the graft and the distal cord stump.
Methods: There were 22 female fisher rats. One segment of 5-mm spinal cord was removed at T9 level. 6 of them (group1) received Schwann cell grafts positioned between transected stumps to test their efficacy to serve as bridges for axonal regeneration. 16 of them (group 2) received gene-treated Schwann cell grafts. All animals survived 4 weeks. Functional result was assessed by BBB behavior test everyweek after surgery. Fast-Blue injection into SC cable one week before perfusion. Immunocytochemistry to detect labeled neurons in cord, brain stem, and cortex. Toluidine blue stain for myelinated axons.
Results: A bridge between the severed stumps had been formed in all animals, as determined by the gross and histological appearance and the ingrowth of propriospinal axons from both stumps. In group 1, near the bridge midpoint there was a mean of 1800 myelinated axons and eight times as many nonmyelinated, ensheathed axons. In group 2, more fibrous tissue surrounding grafted cords were noted. Myelinated axons can hardly find in group 2 animals excepted some unmyelinated axons. Histological examination shows vigorous inflammatory reaction with Macrophage dominant in the bridges.
Conclusions: This study demonstrates that Schwann cell grafts serve as bridges that support regrowth of both ascending and descending axons across a gap in the adult rat spinal cord. The ground substance of gene-treated graft induced foreign body reaction that inhibits axon regeneration. Additional intervention will be required to eliminate this adverse reaction of the ground substance of gene-treated SC graft.
The abstracts were prepared by Professor Jegan Krishnan. Correspondence should be addressed to him at the Flinders Medical Centre, Bedford Park 5047, Australia.
