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PDZ binding of TARPγ-8 controls synaptic transmission but not synaptic plasticity.

The reduction in synaptic transmission and plasticity in mice lacking the hippocampus-enriched AMPA receptor (AMPAR) auxiliary subunit TARPγ-8 could be a result of a reduction in AMPAR expression or of the direct action of γ-8. We generated TARPγ-8Δ4 knock-in mice lacking the C-terminal PDZ ligand. We found that synaptic transmission and AMPARs were reduced in the mutant mice, but extrasynaptic AMPAR expression and long-term potentiation (LTP) were unaltered. Our findings suggest that there are distinct TARP-dependent mechanisms for synaptic transmission and LTP.

Pubmed ID: 22002768

Authors

  • Sumioka A
  • Brown TE
  • Kato AS
  • Bredt DS
  • Kauer JA
  • Tomita S

Journal

Nature neuroscience

Publication Data

November 27, 2011

Associated Grants

  • Agency: NIMH NIH HHS, Id: MH077939
  • Agency: NINDS NIH HHS, Id: NS050570
  • Agency: NINDS NIH HHS, Id: NS065251
  • Agency: NIMH NIH HHS, Id: R01 MH077939
  • Agency: NIMH NIH HHS, Id: R01 MH077939-04
  • Agency: NINDS NIH HHS, Id: R01 NS050570
  • Agency: NINDS NIH HHS, Id: R01 NS050570-03
  • Agency: NINDS NIH HHS, Id: R01 NS065251
  • Agency: NINDS NIH HHS, Id: R01 NS065251-02

Mesh Terms

  • Age Factors
  • Animals
  • Animals, Newborn
  • Biophysics
  • Calcium Channels
  • Electric Stimulation
  • Gene Expression Regulation, Developmental
  • Guanylate Kinase
  • Hippocampus
  • In Vitro Techniques
  • Long-Term Potentiation
  • Membrane Proteins
  • Mice
  • Mice, Transgenic
  • Models, Biological
  • Mutation
  • Neuronal Plasticity
  • PDZ Domains
  • Patch-Clamp Techniques
  • Synaptic Transmission
  • Synaptophysin
  • Synaptosomes