Diabetic retinopathy is the most common complication of diabetes mellitus and one of the leading causes of blindness worldwide among adults. In the development of diabetic retinopathy genetic, metabolic and growth factors play an important role. Despite vascular abnormalities have been considered the principal damage, several evidences indicate that retinal neurons are also altered during diabetes; atrophy of ganglion cells and degeneration of the inner nuclear layer in human retinas were identified early in diabetes.

By the patch-clamp technique in the whole-cell configuration we recorded the electrical activity of retinal ganglion cells (RGCs) from rats in which diabetes was induced by injecting streptozoticin. From the comparison with control rats, we found significant differences in the pattern of RGC spontaneous activity. Moreover, when stimulated by brief current pulses, diabetic RGCs were not able to fire multiple action potentials but generated a single action potential with overshoot at potentials inferior than 0 mV. Action potential amplitude in diabetic retinas were actually significantly smaller than in control. Our experiments show that RGCs from diabetic rats had altered patterns of both spontaneous and stimulated electrical activity. As RGCs code the information processed in the retina into firing rates, the modifications induced by diabetes in RGC electrophysiological properties could contribute to the severe visual impairments that afflict diabetic patients.