Abstract
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.
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Acknowledgements
We thank R. Nicoll (University of California, San Francisco) for providing the γ-8−/− mouse. The monoclonal antibody to SynDIG1 was developed by and/or obtained from the UC Davis/US National Institutes of Health NeuroMab. This work is supported by grants from the National Institute of Mental Health (MH077939 to S.T.) and from the US National Institutes of Health (NS050570 and NS065251 to J.A.K.).
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S.T. and J.A.K. conceived the project and wrote the manuscript. A.S., T.E.B., A.S.K. D.S.B. and S.T. performed all of the experiments and analyzed the results. All of the authors contributed to the final version of the manuscript.
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Sumioka, A., Brown, T., Kato, A. et al. PDZ binding of TARPγ-8 controls synaptic transmission but not synaptic plasticity. Nat Neurosci 14, 1410–1412 (2011). https://doi.org/10.1038/nn.2952
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DOI: https://doi.org/10.1038/nn.2952
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