Kainate receptor activation induces glycine receptor endocytosis through PKC deSUMOylation

Hao Sun, Li Lu, Yong Zuo, Yan Wang, Yingfu Jiao, Wei-Zheng Zeng, Chao Huang, Michael X. Zhu, Gerald W. Zamponi, Tong Zhou, Tian-Le Xu, Jinke Cheng and Yong Li ()
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Hao Sun: Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine
Li Lu: Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine
Yong Zuo: Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine
Yan Wang: Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine
Yingfu Jiao: Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine
Wei-Zheng Zeng: Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine
Chao Huang: Center for Translational Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine
Michael X. Zhu: The University of Texas Health Science Center at Houston
Gerald W. Zamponi: Hotchkiss Brain Institute, The University of Calgary
Tong Zhou: The University of Alabama at Birmingham
Tian-Le Xu: Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine
Jinke Cheng: Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine
Yong Li: Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine

Nature Communications, 2014, vol. 5, issue 1, 1-17

Abstract: Abstract Surface expression and regulated endocytosis of glycine receptors (GlyRs) play a critical function in balancing neuronal excitability. SUMOylation (SUMO modification) is of critical importance for maintaining neuronal function in the central nervous system. Here we show that activation of kainate receptors (KARs) causes GlyR endocytosis in a calcium- and protein kinase C (PKC)-dependent manner, leading to reduced GlyR-mediated synaptic activity in cultured spinal cord neurons and the superficial dorsal horn of rat spinal cord slices. This effect requires SUMO1/sentrin-specific peptidase 1 (SENP1)-mediated deSUMOylation of PKC, indicating that the crosstalk between KARs and GlyRs relies on the SUMOylation status of PKC. SENP1-mediated deSUMOylation of PKC is involved in the kainate-induced GlyR endocytosis and thus plays an important role in the anti-homeostatic regulation between excitatory and inhibitory ligand-gated ion channels. Altogether, we have identified a SUMOylation-dependent regulatory pathway for GlyR endocytosis, which may have important physiological implications for proper neuronal excitability.

Date: 2014
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DOI: 10.1038/ncomms5980

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