Study On The Electrical Stimulation Of Axotomized Retinal Ganglion Cells In Rat Eyes

Adult mammalian central nervous system damage and its repair has always beenhotspot and difficulty in academic research. Injury of central nervous system (CNS)usually leads to permanent defects because of neurons lack the ability to proliferate.Retina and optic nerve are derivatives of CNS. Retina derived from the neuralectoderm and retinal ganglion cells are only in the retina to the projection neurons inthe brain which located in the innermost layer of ganglion cells in the retina. The opticnerve is composed of retinal ganglion cell axons belonging to the white matter of thecentral nervous system. Because of the cell body of retinal ganglion cells (RGCs) andunmyelinated axons can be handled separately, using the tiling technology of the retinacan count the number of retinal ganglion cells in the entire retina. Optic nerve is considered to be one of the most important animal model to study the CNS injury. CNSsuffer from traumatic injury often leads to death and degeneration of the axon of theneuron. A widely variety of attempts have been made to promote neuronal survival andaxonal regeneration of axotomized neurons such as neurotrophic factors, hormones anddrugs. Electrical stimulation (ES) as a physical therapy is widely used for the recoveryafter nervous system injury. ES protective effect can be observed both in the peripheralnervous system and the CNS. It has been shown in vitro and in vivo studies that ESpromotes survival and neurite outgrowth of RGCs. However in short single electricalstimulation in the CNS the number of neuronal survival is limited and not apparent. Inthis study, we use a rat model of optic nerve transection to explore the impact ofchronic electrical stimulation on the survival of RGCs and mechanisms. The first partof the experiment, the study of chronic ES survival of RGCs of the ON transection.Rats were randomly divided into ES group and control group. Exposed and transectedwas performed1.5mm behind the eye-ball. Electrical stimulation was given ES groupafter transection optic nerve. Control group was only transection optic nerve. A smallpiece of gelfoam soaked in a5%gold fluorescent dye was inserted at the site of thestump of the optic nerve, which were retrogradely labeled the RGCs. ES significantlyenhanced RGCs survival at7d and14d after optic nerve transection. Within a certainrange in the electrical stimulation group the closer distance to the pole, the morenumber of surviving RGCs. The second part of the experiment to study the mechanismof protective effects of electrical stimulation of RGCs after optic nerve transection. Weimmunohistochemistry electrical stimulation group and normal control group foundthat in7d and14d of electrical stimulation group microglia expression level wassignificantly reduced and the activation of the microglia was inhibited. Western blotconfirmed that electrical stimulation could inhibit the activity of microglia. Our resultsindicate that chronic electrical stimulation has a protective effect on RGCs after theoptic nerve transection, the mechanism may be to inhibit the activity of microglia.