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Abstract
Jia-Hua Hu1, 6, Joo Min Park1, 6, Sungjin Park1, 6, Bo Xiao1, 5, Marlin H. Dehoff1, Sangmok Kim1, Takashi Hayashi1, 2, Martin K. Schwarz4, Richard L. Huganir1, 2, Peter H. Seeburg4, David J. Linden1 and Paul F. Worley1, 3, *
1 Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
2 Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
3 Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
4 Department of Molecular Neurobiology, Max Planck Institute for Medical Research, 69120 Heidelberg, Germany
5 The State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, P.R. China, 610041
*Corresponding author
6 These authors contributed equally to this work
Summary
Homeostatic scaling is a non-Hebbian form of neural plasticity that maintains neuronal excitability and informational content of synaptic arrays in the face of changes of network activity. Here, we demonstrate that homeostatic scaling is dependent on group I metabotropic glutamate receptor activation that is mediated by the immediate early gene Homer1a. Homer1a is transiently upregulated during increases in network activity and evokes agonist-independent signaling of group I mGluRs that scales down the expression of synaptic AMPA receptors. Homer1a effects are dynamic and play a role in the induction of scaling. Similar to mGluR-LTD, Homer1a-dependent scaling involves a reduction of tyrosine phosphorylation of GluA2 (GluR2), but is distinct in that it exploits a unique signaling property of group I mGluR to confer cell-wide, agonist-independent activation of the receptor. These studies reveal an elegant interplay of mechanisms that underlie Hebbian and non-Hebbian plasticity.
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