Effects Of Transcorneal Electrical Stimulation On The Activities Of Retinal Microglia Cells After Optic Nerve Damage In Rats

PurposeTo investigate the effects of transcorneal electrical stimulation (TES) on the activities of retinal microglia cells (RMGs) and the expression of tumor necrosis factor-α (TNF-α) after optic nerve injury.MethodsTo investigate the effects of TES on the survival of retinal ganglion cells (RGCs) and the activities of RMGs after optic nerve transection (ONT). Ninety adult male Sprague-Dawley (SD) rats were randomly divided into3groups:Control, ONT+Sham, and ONT+TES groups. RGCs were retrograde-labeled by fluorogold (FG) through bilateral superior colliculus for seven days before ONT. The optic nerve (ON) was exposed without being transected in the Control group, sham TES was given to rats in the ONT+Sham group0day,4days or0day,4days,7days,10days after ONT, and TES was given to rats in the ONT+TES group0day,4days or0day,4days,7days,10days after ONT. Seven or14days after ONT, the retinas were dissected from the eyes and the number of RGCs and RMGs was counted using immunofluorescence technique. In addition, double fluorescence labeling was used to identify whether TNF-a and RMGs were colocalized in the retinas and the expression of TNF-a was assayed by western blot.ResultsCompared with the Control group, the number of RGCs in the ONT+Sham group and the ONT+TES group markedly decreased7days or14days after ONT, while the number of RMGs markedly increased. RMGs also responded to ONT by transformation from resting to active states. The number of RGCs in the ONT+TES group was more than those in the ONT+Sham group7days or14days after ONT. Both the number of RMGs and amoeboid RMGs in the ONT+TES group were less than those in the ONT+Sham group7days after ONT. Although the difference of the number of RMGs between two groups was not significant14days after ONT, the number of amoeboid RMGs in the ONT+TES group was still less than those in the ONT+Sham group. Double fluorescence labeling revealed that TNF-a was colocalized with amoeboid RMGs7days after ONT, however,14days after ONT, TNF-a was colocalized with all form of RMGs. In addition, TES suppressed the expression of TNF-a7days or14days after ONT. ConclusionOur work demonstrated that optic nerve damage would active RMGs and improve the expression of TNF-a. TES may prevent RGCs loss after optic nerve damage via suppressing the activation of RMGs and reducing the expression of TNF-a.