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Homeostatic scaling requires group I mGluR activation mediated by Homer1a.

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.

Pubmed ID: 21172614

Authors

  • Hu JH
  • Park JM
  • Park S
  • Xiao B
  • Dehoff MH
  • Kim S
  • Hayashi T
  • Schwarz MK
  • Huganir RL
  • Seeburg PH
  • Linden DJ
  • Worley PF

Journal

Neuron

Publication Data

December 22, 2010

Associated Grants

  • Agency: NIDA NIH HHS, Id: DA010309
  • Agency: NIDA NIH HHS, Id: DA011742
  • Agency: NIMH NIH HHS, Id: MH084020
  • Agency: NINDS NIH HHS, Id: NS036715
  • Agency: NIDA NIH HHS, Id: R01 DA011742
  • Agency: NIDA NIH HHS, Id: R01 DA011742-13
  • Agency: NIDA NIH HHS, Id: R37 DA010309
  • Agency: NIDA NIH HHS, Id: R37 DA010309-16

Mesh Terms

  • Animals
  • Carrier Proteins
  • Cells, Cultured
  • Cerebral Cortex
  • Excitatory Postsynaptic Potentials
  • Homeostasis
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Neuronal Plasticity
  • Receptors, Metabotropic Glutamate
  • Signal Transduction