Graft derived reafferentation of host spinal cord is not necessary for amelioration of lesion-induced deficits: Possible role of migrating grafted astrocytes

Abstract

The present study explores the ability of fetal spinal cord homografts into lesioned host C3 fasiculus gracilis to influence the expected deterioration of hindlimb performance following this lesion. Rats were trained to traverse a narrow platform for a water reward. Animals were ranked for hindlimb performance utilizing slips, recovery and manner of traversing the platform. After training the animals, numbers were recoded, laminectomy performed at C3 and subject fasiculus gracilis (FG) bilaterally aspirated. Half the subjects were randomly selected for implantation of two, one mm segments of 14 day gestation cervical spinal cord. Recoded lesion-only and lesion-transplanted animals were tested 21, 30, 45, 60 and 90 days later. C3 fetal transplants significantly decreased the severity of hindlimb deficit at 21 and 90 days postlesion ( p < 0.05). The C1-FG of both groups contained no nerve fibers. However, the host nucleus gracilis of lesion-transplant animals contained normal sizes and numbers of neurons whereas the lesion-only group did not. This neuronal maintenance may have been due to factor(s) secreted by transplant derived astrocytes which migrated at 0.72–0.76mm/day and reside in the host nucleus gracilis.