Two mutations preventing PDZ–protein interactions of GluR1 have opposite effects on synaptic plasticity | Zendy

Jannic Boehm | Zendy; Ingrid Ehrlich | Zendy; Helen Hsieh | Zendy; Roberto Malinow | Zendy

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Two mutations preventing PDZ–protein interactions of GluR1 have opposite effects on synaptic plasticity

Author(s) -

Jannic Boehm,

Ingrid Ehrlich,

Helen Hsieh,

Roberto Malinow

Publication year - 2006

Publication title -

learning and memory

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.228

H-Index - 136

eISSN - 1549-5485

pISSN - 1072-0502

DOI - 10.1101/lm.253506

Subject(s) - pdz domain , synaptic plasticity , plasticity , neuroscience , long term potentiation , ligand (biochemistry) , microbiology and biotechnology , mutation , chemistry , biology , phenotype , genetics , receptor , gene , physics , thermodynamics

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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