The cell adhesion molecule Sdk1 shapes assembly of a retinal circuit that detects localized edges

Nearly 50 different mouse retinal ganglion cell (RGC) types sample the visual scene for distinct features. RGC feature selectivity arises from their synapses with a specific subset of amacrine (AC) and bipolar cell (BC) types, but how RGC dendrites arborize and collect input from these specific subsets remains poorly understood. Here we examine the hypothesis that RGCs employ molecular recognition systems to meet this challenge. By combining calcium imaging and type-specific histological stains, we define a family of circuits that express the recognition molecule Sidekick-1 (Sdk1), which include a novel RGC type (S1-RGC) that responds to local edges. Genetic and physiological studies revealed that Sdk1 loss selectively disrupts S1-RGC visual responses, which result from a loss of excitatory and inhibitory inputs and selective dendritic deficits on this neuron. We conclude that Sdk1 shapes dendrite growth and wiring to help S1-RGCs become feature selective.

Automated summary

This study explores how nearly 50 different mouse retinal ganglion cell (RGC) types use molecular recognition systems, specifically the recognition molecule Sidekick-1 (Sdk1), to become feature selective. Loss of Sdk1 disrupts the visual responses of a specific RGC type (S1-RGC) by affecting excitatory and inhibitory inputs as well as dendritic deficits. The findings suggest that Sdk1 shapes dendrite growth and wiring to help RGCs become feature selective.