Abstract
The regulated trafficking of GluR1 contributes significantly to synaptic plasticity, but studies addressing the function of the GluR1 C-terminal PDZ-ligand domain in this process have produced conflicting results. Here, we resolve this conflict by showing that apparently similar C-terminal mutations of the GluR1 PDZ-ligand domain result in opposite physiological phenotypes during activity- and CamKII-induced synaptic plasticity.
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Dates
Type | When |
---|---|
Created | 18 years, 11 months ago (Sept. 15, 2006, 8:55 p.m.) |
Deposited | 3 years, 9 months ago (Nov. 11, 2021, 9:34 a.m.) |
Indexed | 1 year, 7 months ago (Jan. 16, 2024, 9:02 a.m.) |
Issued | 18 years, 11 months ago (Sept. 1, 2006) |
Published | 18 years, 11 months ago (Sept. 1, 2006) |
Published Online | 18 years, 11 months ago (Sept. 15, 2006) |
Published Print | 18 years, 11 months ago (Sept. 1, 2006) |
@article{Boehm_2006, title={Two mutations preventing PDZ–protein interactions of GluR1 have opposite effects on synaptic plasticity}, volume={13}, ISSN={1549-5485}, url={http://dx.doi.org/10.1101/lm.253506}, DOI={10.1101/lm.253506}, number={5}, journal={Learning & Memory}, publisher={Cold Spring Harbor Laboratory}, author={Boehm, Jannic and Ehrlich, Ingrid and Hsieh, Helen and Malinow, Roberto}, year={2006}, month=sep, pages={562–565} }