| Injury and recovery of central nervous system are the focal point and nodus in the academic circles. Injury of central nervous system usually leads to neurocyte death and nonreversible axon degeneration in adult mammal. RGCs belongs to central nervous system , and the characters of RGCs are similar as neurons of central nervous system . Many studies about central nervous system have been carried out using the transection of optic nerve as model system. Electrical stimulation is a kind of treatment to injury in peripheral nervous system. It has been reported that electrical stimulation can induce axotomized sciatic nerve to extend axons in vivo and in vitro. Moreover, chronic electrical stimulation by a cochlear implant promotes survival of spiral ganglion neurons after neonatal deafness, and electrical stimulation enhances the survival of axotomized retinal ganglion cells in vivo. In central nervous system , it is reported that transcorneal electrical stimulation rescues axotomized retinal ganglion cells by activating endogenous retinal IGF-1 System. In the first part of this study, we investigated the neuroprotective effect of delayed and repeated electrical stimulation on axotomized RGCs in adult rats . Our result showed that delayed and repeated electrical stimulation could enhance the survival of axotomized RGCs in adult rats. Treatment with electrical stimulation at the third day or the fifth day after ON transection induced a significant increase in the number of FG-labeled RGCs, when compared with the control animals. Electrical stimulation was carried on at the third day after ON axotomy, and the neuroprotective effect kept on 11 days. We performed ES repeatly, once every 3 days, from 0 day to the 14th day after ON axotomy. The survival number of RGCs was more than those without ES at the third day. Given these lines of evidence, we hypothesized that delayed electrical stimulation may improve the survival of axotomized RGCs in vivo. To test this hypothesis, in the present study, we examined, on day 7 after ON transection, the level of IGF-1 in the retinas with or without electrical stimulation 3 days after ON transection in adult rats. The express of IGF-1 in Müller cells with ES was more than those without ES. This indicate that ES activate IGF-1 system and promote the survival of RGCs. To test the state of Müller cells , we examined, on day 7 after ON transection, the level of GFAP in the retinas with or without electrical stimulation 3 days after ON transection in adult rats. The express of GFAP in Müller cells with ES was more than those without ES. This indicated that ES activated Müller cells and promoted the survival of RGCs. The reaction was not conspicuous in astrocyte. We also found the inhibition effect induced by ES in microglias, and those reduced the damage to RGCs. The direct effect to RGCs induced by ES was observed in our experiment. p-Akt signal pathway was activate by ES in RGCs, and apoptosis of RGCs was inhibited. Therefore, TsES was a useful neuroprotective method for clinical research, and the mechanism of TsES was complex. |
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