Department of Physiology, McGill University, Montreal, Canada.
Elife. 2021 Sep 21;10:e70870. doi: 10.7554/eLife.70870.
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.
近 50 种不同的小鼠视网膜神经节细胞 (RGC) 类型对不同的视觉特征进行采样。RGC 的特征选择性源于它们与特定的一部分无长突细胞 (AC) 和双极细胞 (BC) 类型的突触,但 RGC 树突如何分支并从这些特定的亚群中收集输入仍然知之甚少。在这里,我们检验了一个假设,即 RGC 利用分子识别系统来应对这一挑战。通过结合钙成像和特定类型的组织学染色,我们定义了一组表达识别分子 Sidekick-1 (Sdk1) 的电路,其中包括一种对局部边缘有反应的新型 RGC 类型 (S1-RGC)。遗传和生理学研究表明,Sdk1 的缺失选择性地破坏了 S1-RGC 的视觉反应,这是由于兴奋性和抑制性输入的丧失以及该神经元选择性的树突缺陷所致。我们的结论是,Sdk1 塑造了树突的生长和连接,帮助 S1-RGC 实现特征选择性。