Pathological Retinal Oscillations across Retinal Diseases: Shared Circuit Mechanisms and Implications for Photopsia

Abstract

Retinitis pigmentosa (RP) is an inherited retinal disorder characterized by the progressive degeneration of photoreceptor cells, representing a leading cause of blindness. A substantial proportion of patients with RP report photopsia—the perception of spontaneous flashes of light in the visual field. Photopsia can act as visual “noise” and may interfere with visual processing, even compromising restored visual signals following emerging therapeutic interventions. In retinal degeneration (rd) animal models, retinal ganglion cells (RGCs) exhibit pathological periodic spontaneous firing, or oscillations, which have been implicated as a retinal circuit substrate for photopsia. In this review, we summarize current findings on pathological retinal oscillations in rd models and incorporate recent evidence from congenital stationary night blindness (CSNB) models. Together, these studies suggest that RGC oscillations are not simply a consequence of photoreceptor degeneration, but instead arise from a pathological state of the ON bipolar cell–AII amacrine cell network associated with TRPM1-dependent signaling. We propose that altered input balance within this network, including reduced rod bipolar cell-to-AII amacrine cell signaling and altered ON cone bipolar cell activity, may represent a shared mechanism underlying pathological oscillations across distinct retinal diseases.