Two mutations preventing PDZ–protein interactions of GluR1 have opposite effects on synaptic plasticity
- Jannic Boehm1,3,
- Ingrid Ehrlich1,3,
- Helen Hsieh1,2,3, and
- Roberto Malinow1,2,4
- 1 Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA;
- 2 Department of Neurobiology and Behavior, SUNY Stony Brook, Stony Brook, New York 11794, USA
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↵3 These authors contributed equally to this work.
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.
Footnotes
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↵4 Corresponding author.
↵4 E-mail malinow{at}cshl.edu; fax (516) 367-8372.
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Article published online before print. Article and publication date are at http://www.learnmem.org/cgi/doi/10.1101/lm.253506
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- Received March 16, 2006.
- Accepted June 13, 2006.
- Copyright © 2006, Cold Spring Harbor Laboratory Press
