Establishment Spinal Cord Injury Model And Assessment Of Functional Recovery And Spinal Cord Axonal Regeneration In NB-3 Null Mice

Repairing of spinal cord injury (SCI) has aways been a challenge in the field of neuroscience. The main reason is that axon regeneration after SCI is very limited. It is difficult to break through the glial scar, establish synaptic linkages with previous target cells, resume innervation to the target cells and promote the functional recovery of target organs. Previous studies have shown that manipulating gene expression, removing inhibitory factors, injecting neurotrophins and other growth factors can promote axon regeneration, but with limited success. In recent years, inhibitory factor has become a hotspot in the field of axonal regeneration. In addition to the traditional glial scar and myelin associated inhibitory factors (MAIFs), the mechanisms of axon guidance molecules, neural adhesion molecules and tumor suppressors on neural inhibition of axonal regeneration have been clarified. Therefore remove these inhibitors will be conducive to the axon regeneration and the neural functional recovery. In our research, we establish spinal cord injury model and by using yellow fluorescent protein (YFP-H) mouse and DiI tracing to observe the regeneration of CST axon in adult NB-3 knock out mouse after spinal cord injury. The BMS, BBB locomotor rating scale was used to assess functional recovery. Our research indicate that NB-3 knochout mouse has potential for CST axon regeneration and motor functional recovery. In conclusion, the neural recognition molecule NB-3 can directly or indirectly suppress axon regeneration in central nervous system (CNS) and provide clues for more reseach on axon regeneration after spinal cord injury.