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.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Age Factors
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Animals
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Animals, Newborn
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Biophysics
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Calcium Channels / genetics
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Disks Large Homolog 4 Protein
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Electric Stimulation
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Gene Expression Regulation, Developmental / genetics
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Guanylate Kinases / metabolism
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Hippocampus / cytology
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Hippocampus / drug effects
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In Vitro Techniques
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Long-Term Potentiation / drug effects
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Long-Term Potentiation / genetics
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Membrane Proteins / genetics
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Membrane Proteins / metabolism*
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Mice
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Mice, Transgenic
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Models, Biological
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Mutation / genetics
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Neuronal Plasticity / genetics
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Neuronal Plasticity / physiology*
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PDZ Domains / genetics
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PDZ Domains / physiology*
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Patch-Clamp Techniques
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Synaptic Transmission / genetics
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Synaptic Transmission / physiology*
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Synaptophysin / metabolism
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Synaptosomes / metabolism
Substances
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Cacng2 protein, mouse
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Calcium Channels
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Disks Large Homolog 4 Protein
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Dlg4 protein, mouse
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Membrane Proteins
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Synaptophysin
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TARP gamma-8 protein, mouse
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Guanylate Kinases