| BackgroundsIt was well established that the adult mammalian spinal axons could not regenerate after injury because of the inhibiting environment and the inefficient intrinsic regenerating capacity of spinal cord itself. Nevertheless, there was not efficient functional repairment of SCI yet no matter that the monoclonal antibody IN-1, immunization or gene knockout was applied in. So it might be necessary for repairing spinal cord injury to reinforce the intrinsic regenerating capacity of spinal cord . As a messenger, cAMP simulated the outgrowth of neuronal processes in the inhibiting culture medium and induced the axonal regeneration in vivo. It also mediated the function of neurotrophic factors stimulating the axonal growth. Besides these, Neuronal cAMP controlled the developmental loss in ability of axons to regenerate. So,it was proposed that cAMP could reinforce the intrinsic regenerating capacity of spinal cord by the cellular signalling pathway.It was widely accepted that spontaneous locomotion recovery after SCI existed in the rodent animals. The regulation of BBB scale was most widely used in evaluating the SCI and its repairing effect though it didn't distinguish the initiative or spontaneous hindlimb movements. It would make the regulation of BBB scale more exactly and precisely reflecting the effect of repairing strategy to distinguish and exclude the spontaneous locomotion recovery from the hindlimb movements recovery after SCI. That would redound to provide more reliable data for the researches on SCI.Objectives1. To explore whether cAMP input in vivo could induce axonal regeneration and repair SCI.2. To investigate what level the spontaneous locomotion recovery could get to after SCI in rats.Methods1. 56 Rats models of spinal cord dorsal hemisection adopted and dibutyryl-cAMP injected in the motor cortex once or continuously input in the lesion site or in the subarachnoid cistern for three days. The distribution of NFs in the lesion area was observed by immunohistochemistry. Corticospinal tracts and spinal axons regeneration was investigated by CST and spinal axons anterograded tracing with BDA. The function of hindlimb movements were evaluated in BBB scales and as a reference to evaluate the repairing effect of treating strategy.2. Four groups of spinal cord injury rat models including T10 dorsal half hemisection, T10 transection ,T10 segment resection, T10-L4 segments resection were adopted. Histological examinations and BBB scales of hindlimb movements were observed. The relationship between the function of hindlimb movements recovery after SCI and BBB scales was evaluated.Results1. When cAMP was continuously input in the subarachnoid cistern, more NFs presented in the lesison area and more labelled CST fibers presented in the rostral of the lesion sites in cAMP group than those in the control group, but there was no obvious axonal regeneration in the lesion area either in cAMP group or in control group. No significance existed between the cAMP group and controlgroup comparing the time curves of BBB scale of hindlimb movements.2. When cAMP was continuously input in the lesion site, more NFs presented in the lesison area in cAMP than that in the control group. A large numbers of spinal axons regeneration ,including some CST axons regeneration were presented in the lesion in cAMP group in spite of no longer continuous axonal regeneration traversing the lesion area to the caudal comparing no axonal regeneration in control group. No significance existed between the cAMP group and control group comparing the time curves of BBB scale of hindlimb movements.3. When cAMP was injected once in the brain motor cortex, more NFs presented and distributed more evenly in the lesison area in cAMP than that in the control group. Some regenerated axons presented in the lesion area and wandered along the edge of cysts to the caudal and some ventral axons regenerated into the the dorsal dense scars from the rostral to the caudal in cAMP group comparing no axonal regene...
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