Rac1 Modulates Excitatory Synaptic Transmission in Mouse Retinal Ganglion Cells.
10.1007/s12264-019-00353-0
- Author:
Ling-Zhu LI
1
;
Ning YIN
1
;
Xue-Yan LI
1
;
Yanying MIAO
1
;
Shuo CHENG
1
;
Fang LI
1
;
Guo-Li ZHAO
1
;
Shu-Min ZHONG
1
;
Xin WANG
1
;
Xiong-Li YANG
1
;
Zhongfeng WANG
2
Author Information
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.
2. 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. zfwang@fudan.edu.cn.
- Publication Type:Journal Article
- Keywords:
Dendrite;
Dendritic spine;
Excitatory synaptic transmission;
Rac1;
Retinal ganglion cell
- From:
Neuroscience Bulletin
2019;35(4):673-687
- CountryChina
- Language:English
-
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/GABA receptor-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.
