Influence Of Transcorneal Electrical Stimulation On Light Exposed Rats

Abstract

Purpose: : Neuroprotective effects of transcorneal electrical stimulation (TES) have been described for a variety of circumstances such as optic nerve crush and retinal dystrophies, but mechanisms have not yet been thoroughly established. In this study we assessed the effect of TES on retinal degeneration caused by light damage (LD) in rats.

Methods: : 45 Sprague Dawley rats (mean weight 213.82 ± 17.3 g) were examined using electrophysiological (electroretinography; ERG) and morphological (histology) approaches. All rats underwent baseline measurements at the beginning of the study for intra-individual comparison. Rats were divided into three groups: (1) EST: LD and TES (n=15); (2) SHAM: LD and sham-stimulation (n=15); (3) CNTR: only LD (n=15) one week after baseline measurement. ERGs were recorded weekly for 3 weeks post treatment.

Results: : No significant differences were found at baseline measurements between all groups. Differences were measured in several ERG values (a-wave, b-wave amplitudes, oscillatory potentials and a-wave slope of different stimulation intensities [0.001-30 cd.s/m²]) and in parameters of a scotopic fit (0.000003-60 cd.s/m²) between EST, SHAM and CNTR, where the EST group shows higher ERG potentials than SHAM and CNTRL group in the first week after LD (maximum response of scotopic fit ANOVA p = 0.009). A reversible effect of LD was detected in week two and three after LD. The differences between EST, SHAM and CNTR group were smaller than in the first week after treatment, but with a tendency for EST group for higher amplitudes (maximum response of scotopic fit in week 2 ANOVA p = 0.042). No significant differences were found in photopic ERG measurements. Retinal histology showed a significant ONL thickness preservation in the TES group compared to SHAM and CNTR groups. In these groups, after LD the superior retina was more severely damaged than the inferior retina.

Conclusions: : TES can protect photoreceptor cells against light-induced degeneration. Application of TES in human retinal degenerative diseases could be a method to decelerate or protect against photoreceptor cell death and open new therapeutic perspectives.

Keywords: neuroprotection • electrophysiology: non-clinical • protective mechanisms