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The nerve regeneration mechanisms are very important. If the mechanism were obviously defined and found the primary cause, those caused patients suffer from nerve injury to live more than yet. In fact, the factor affected regeneration is diverse. We are willing to review that electrical stimulation affects nerve regeneration. Specifically, we review that electrical stimulation affects velocity and regeneration mechanism related genetic factor. Neural regeneration speed was studied by radioisotope labeling of transported proteins and by anterograde labeling of regenerating axons, and was not altered by electrical stimulation. Attempts to condition the neuron by stimulating the femoral nerve 1 week before injury were also without effect. Electrical stimulation thus promotes the onset of motor axon regeneration without increasing its speed. This finding suggests a combined approach to improving the outcome of nerve repair. Additionally, in the study, we investigated whether electrical stimulation accelerates the upregulation of T®1-tubulin and GAP-43(regeneration-associated genes : RAGs) and the downregulation of the medium-molecular-weight neurofilament (NFM) on genetic factor related regeneration mechanism. 1. two weeks prior to unilateral femoral nerve transection and suture, fluorogold (Fluorochrome Inc., Denver) or fluororuby (Dextran tetramethylrhodamine, Mol.
Probes, D-1817, Eugene, OR) was injected into quadriceps muscles. 2. Over a period of 7 days, fresh spinal cords were processed for semiquantitation of mRNA by using in situ hybridization. 3. There was an increase in T®1-tubulin and GAP-43 mRNA and a decline in the NFM mRNA at 7 days after nerve suture and sham stimulation but not in intact nerves. In contrast, 1 hr stimulation of sutured but not intact nerves dramatically accelerated the changes in gene expression. The changes in RAGs and NFM gene expression were delayed relative to the accelerated upregulation of BDNF and trkB mRNA by electrical stimulation. The temporal sequence of upregulation of BDNF and trkB, altered gene expression of RAGs and NFM, and accelerated axonal outgrowth from the proximal nerve stump are consistent with a key role of BDNF and trkB in mediating the altered expression of RAGs and, in turn, the promotion of axonal outgrowth after electrical stimulation. Taken together, as mentioned above, the ratio of nerve growth is strikingly increased by electrical peripheral nerve stimulation, which implicated that it might be applicable therapeutics for neural repair and regeneration as well as functional rehabilitation as traditional physical therapeutics.