Cell firing between ON alpha retinal ganglion cells and coupled amacrine cells in the mouse retina

Abstract

Gap junctions are channels that allow for direct transmission of electrical signals between cells. However, the ability of one cell to be impacted or controlled by other cells through gap junctions remains unclear. In this study, heterocellular coupling between ON α retinal ganglion cells (RGCs) and displaced amacrine cells (ACs) in the mouse retina was utilized as a model. The impact of the extent of coupling of interconnected ACs on the synchronized firing between coupled ON α RGC-ACs pairs was investigated. It was observed that the synchronized firing between the ON α RGC-ACs pairs was increased by the dopamine 1 receptor antagonist SCH23390, while it was eradicated by the agonist SKF38393. Subsequently, coupled ON α RGC-AC pairs were infected with the channelrhodopsin-2(ChR2) mutation L132C. The spikes of ON α RGCs (without ChR2) could be triggered by ACs (with ChR2) through the gap junction, and vice versa. Furthermore, it was observed that ON α RGCs stimulated with 3-10 Hz currents by whole-cell patch could elicit synchronous spikes in the coupled ACs, and vice versa. The study implies that the synchronized firing between ON α RGC-AC pairs could potentially be affected by the coupling of interconnected ACs, and another cell type could selectively control the firing of one cell type, and information could be forcefully transmitted. The key role of gap junctions in synchronizing firing and driving cells between α RGCs and coupled ACs in the mouse retina is highlighted.