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

Nature neuroscience | Nov 27, 2011

http://www.ncbi.nlm.nih.gov/pubmed/22002768

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 RIS Download

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

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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

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