The Model Of Spinal Cord Injury

Functional deficits following SCI result fromdamage to or severance of axons, loss of neurons and glia, anddemyelination. SCI pathology is determined not only by the initial mechanical insult, but also by secondary processes including ischemia, anoxia, free - radical formation, and excitotoxicity that occur over hours and days following injury. Central nervous system (CNS) axonal regeneration appears to be impeded partly by myelin - associated inhibitors , loss in adult neurons of an intrinsic ability to overcome inhibitory cues , and formation of a post - lesion scar barrier. However, if axons can traverse the injury site, there is evidence that they may regrow in unscarred regions . Furthermore, preservation of even a small percentage of tissue significantly enhances functional recovery . Although there have been encouraging reports of deficit reduction and axonal regrowth by blocking inhibitory molecules and antagonizing secondary injury mechanisms ; myelin replacement by stem , Schwann , and olfactory en-sheathing cells ; delivery of growth factors and small molecules ; and implantation of fetal tissue and scaffolds , as yet there is no practical treatment for SCI.We sought a conceptually new approach that simulated the architecture of the spinal cord injury through Hemisection of the spinal cord . The spinal cord of T9 -10 was desection by microsurgery. And the functional recover was valued by scores of BBB. The H&E stains was done using the slide of spinal cord at 8 week post operation. ANOVA was used to value the significant of the data.