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Two mutations preventing PDZ-protein interactions of GluR1 have opposite effects on synaptic plasticity
Jannic Boehm1, Ingrid Ehrlich, Helen Hsieh
1Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA.
Learning & Memory (Cold Spring Harbor, N.Y.)
|September 19, 2006
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.

