New research reveals that the loss of a single ion channel, TRPM1, is enough to produce persistent rhythmic oscillations in the retina, a feature observed in both congenital stationary night blindness and retinitis pigmentosa. By comparing Trpm1 and mGluR6 knockout mice, researchers identified a disrupted circuit between rod bipolar cells and AII amacrine cells that produces anti-phase oscillations interfering with visual signaling.