Using a novel phospho-deficient GluA2 Y876F knockin mice, the paper’s lead author, Adeline Yong, showed that phosphorylation of the AMPAR subunit, GluA2, at tyrosine-876 is required for homeostatic synaptic strengthening by dictating GluA2 binding to GRIP1, a scaffolding protein crucial for synaptic upscaling. This finding provides an understanding of the mechanism through which a neuron can maintain a range of synaptic signaling whilst not compromising its responsiveness to subsequent synaptic activity. Read the full article here.