Diabetes can result in diabetic retinopathy, causing abnormal color vision and decreased contrast sensitivity, effects that have been consistently replicated in diabetic rodent models. Doctors had previously thought the impairment of vision came from damage to the blood vessels induced by high blood sugar, but it is increasingly recognized that retinal dysfunction predates such vascular lesions.

Retinal dopamine directly modulates multiple aspects of vision through activation of selective receptors and retinal pathways. Disruption in the retinal dopaminergic system has been observed in diabetes, though its potential contribution to the pathogenesis of diabetic retinopathy remains unclear. New research elucidates this contribution and suggests that a dopamine-restoring drug already used to treat Parkinson's disease, called L-DOPA, may also be used to treat diabetic retinopathy.

Researchers led by Machelle Pardue (Atlanta VA Medical Center, GA) and Michael Iovone (Emory University, Atlanta, GA) studied rats and mice made diabetic by treating them with streptozotocin (STZ), a substance that is toxic to insulin-producing cells in the pancreas. The induced diabetes significantly reduced retinal dopamine levels by 4 weeks or 5 weeks after STZ injections in rats and mice, respectively. Next, they tested the vision of diabetic mice by placing them on a platform surrounded by four computer screens that displayed rotating black and white lines. Spatial acuity was assessed by gradually making the lines finer, and contrast sensitivity was determined by reducing the contrast between the black and white lines, both until the mice stopped tracking the rotating lines. Diabetic mice showed both reduced spatial frequency thresholds and reduced contrast sensitivities.

In another experiment, mice with dopamine selectively deleted in the retina also showed reduced spatial acuity and contrast sensitivity, confirming the key role of dopamine in vision. When these mice were made diabetic with STZ, their vision did not deteriorate further, confirming that the visual dysfunction seen in diabetic mice is linked to a loss of dopamine.

In contrast, treating the diabetic mice with L-DOPA delayed and mitigated the visual deficits; spatial frequency thresholds only diminished after 4 weeks, and contrast sensitivities only after 6 weeks (J. Neurosci. 34, 726–736; 2014). L-DOPA treatment also rescued the visual impairments of the mice genetically lacking retinal dopamine by restoring levels to those of control mice.

Said Pardue of the findings, “There was some evidence already that dopamine levels were reduced in diabetic retinopathy, but what's new here is we can restore dopamine levels and improve visual function in an animal model of diabetes.”