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Nat Neurosci. 2011 Oct 16;14(11):1410-2. doi: 10.1038/nn.2952.

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

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1
Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, Connecticut, USA.

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.

PMID:
22002768
PMCID:
PMC3206644
DOI:
10.1038/nn.2952
[Indexed for MEDLINE]
Free PMC Article
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