Abstract
The C-terminal PDZ ligand of the AMPA receptor GluR1 subunit may be important for expression of CA1 hippocampal long-term potentiation. To test this directly in vivo, we generated a knock-in mouse lacking the last seven residues of GluR1, comprising the PDZ ligand. This deletion did not affect basal GluR1 synaptic localization, basal synaptic transmission, long-term potentiation or long-term depression, indicating that the ligand is not required for CA1 hippocampal synaptic plasticity.
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Acknowledgements
This work was supported by US National Institutes of Health grant NS36715 and the Howard Hughes Medical Institute.
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Under a licensing agreement between Upstate Group, Inc. and the Johns Hopkins University, R.H. is entitled to a share of royalty received by the University on sales of products described in this article. R.H. is a paid consultant to Upstate Group, Inc. The Johns Hopkins University in accordance with its conflict of interest policies is managing the terms of this arrangement.
Supplementary information
Supplementary Fig. 1
Generation of GluR1Δ7 mice. (PDF 1678 kb)
Supplementary Fig. 2
Synaptic properties of CA1 pyramidal neurons of GluR1Δ7 mice. (PDF 3549 kb)
Supplementary Fig. 3
Pairing-induced LTP is NMDAR- and CaMK II-dependent. (PDF 3113 kb)
Supplementary Fig. 4
Generation of GluR1 knockout mice. (PDF 6138 kb)
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Kim, CH., Takamiya, K., Petralia, R. et al. Persistent hippocampal CA1 LTP in mice lacking the C-terminal PDZ ligand of GluR1. Nat Neurosci 8, 985–987 (2005). https://doi.org/10.1038/nn1432
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DOI: https://doi.org/10.1038/nn1432
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