volume 35, Issue 4, 2019


Rac1 Modulates Excitatory Synaptic Transmission in Mouse Retinal Ganglion Cells

 Ling-Zhu Li1 • Ning Yin1 • Xue-Yan Li• Yanying Miao1 • Shuo Cheng1 • Fang Li1 • Guo-Li Zhao1 • Shu-Min Zhong1 • Xin Wang1 • Xiong-Li Yang1 • Zhongfeng Wang 1


Department of Neurology, Institutes of Brain Science, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Zhongshan Hospital, Fudan University, Shanghai 200032, China

 

Abstract 

 

Ras-related C3 botulinum toxin substrate 1 (Rac1), a member of the Rho GTPase family which plays important roles in dendritic spine morphology and plasticity, is a key regulator of cytoskeletal reorganization in dendrites and spines. Here, we investigated whether and how Rac1 modulates synaptic transmission in mouse retinal ganglion cells (RGCs) using selective conditional knockout of Rac1 (Rac1-cKO). Rac1-cKO significantly reduced the frequency of AMPA receptor-mediated miniature excitatory postsynaptic currents, while glycine/GABAAreceptor-mediated miniature inhibitory postsynaptic currents were not affected. Although the total GluA1 protein level was increased in Rac1-cKO mice, its expression in the membrane component was unchanged. Rac1-cKO did not affect spine-like branch density in single dendrites, but significantly reduced the dendritic complexity, which resulted in a decrease in the total number of dendritic spine-like branches. These results suggest that Rac1 selectively affects excitatory synaptic transmission in RGCs by modulating dendritic complexity.

 

Keywords

Rac1; Retinal ganglion cell; Excitatory synaptic transmission; Dendrite; Dendritic spine ;

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