What is it about?
People with congenital stationary night blindness (CSNB) often experience nystagmus, which causes involuntary eye movements and reduced vision. While traditionally thought to originate in the brain's control circuits, our previous research shows these movements are actually triggered by abnormal rhythmic electrical signals starting in the retina. By studying a mouse model of CSNB, we found that dopamine signaling successfully stops this unwanted retinal "noise" and increased the strength of the signal leaving the retina. This potentially offers a dual benefit: quieting the signals that cause abnormal eye movements while simultaneously sharpening visual acuity. Building on long-standing research into both retinal circuits and the brain's accessory optic system, these findings pave the way for new treatment strategies. Whether delivered through eye drops or systemic dopaminergic substrates, this approach could eventually help patients with nystagmus associated with CSNB and potentially other conditions like albinism, Parkinson's, and retinitis pigmentosa.
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Why is it important?
While our previous research established that infantile nystagmus in congenital stationary night blindness (CSNB) originates from pathological oscillations in the retina, the cellular mechanism driving this instability remained unknown. This study uniquely uncovers that this oscillatory activity is strongly modulated by dopaminergic input to a specific retinal cell type, the AII amacrine cell. This finding is highly significant because it introduces a direct, accessible pharmacological target for a debilitating condition that currently has no cure. By demonstrating that pharmacologically activating D1 dopamine receptors completely suppresses the aberrant retinal "noise" and substantially improves the signal quality of the retina's output neurons, our work lays the critical foundation for developing non-invasive treatments, such as targeted eye drops. Furthermore, this strategy of stabilizing retinal output by modulating dopamine may have broad clinical potential for treating other retinal disorders associated with nystagmus and impaired vision, such as albinism, Parkinson's, and retinitis pigmentosa.
Perspectives
It was a thrilling experience to see the pathological oscillations disappearing live. I thought something went wrong during the experiment. But as the realization set in that dopamine was responsible for controlling these oscillations, it became one of the most profound moments of my career. We did not start this project with a clinical treatment in mind; rather, this discovery grew out of detailed, fundamental research into eye-movement control led by Prof. Chris de Zeeuw and retinal circuits led by Prof. Maarten Kamermans, who sadly passed away recently. Seeing our curiosity-driven basic research unexpectedly yield a potential strategy to treat a condition that currently has no cure is a powerful reminder of why fundamental research is so vital.
B. Semihcan Sermet
Erasmus Universiteit Rotterdam
Read the Original
This page is a summary of: Dopamine suppresses pathological retinal oscillations and enhances the signal-to-noise ratio, Proceedings of the National Academy of Sciences, October 2026, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2535572123.
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