Abstract
Long-term depression (LTD) is a reduction in the efficacy of neuronal synapses, but the molecular basis of LTD signaling and how these signals lead to phenotypic outcomes, such as the shrinkage of synaptic regions, is not clear. In a new report, Woolfrey et al use chemically-induced LTD and a multitude of in vitro biochemical assays to provide evidence that synaptic removal of the scaffolding protein AKAP79/150 promotes LTD-induced spine shrinkage. The further identification of CaMKII, a kinase primarily associated with long-term potentiation (LTP), as a requirement for AKAP79/150 removal, uncovers unexpected interplay between different post-translational modifications and points to a new model of LTD.