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

The regulated trafficking of GluR1 contributes significantly to synaptic plasticity, but studies addressing the function of the GluR1 C-terminal PDZ-Iigand 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.