Synaptic plasticity is known to underlie learning and memory, but we're still discovering the molecular mechanisms by which synaptic activity leads to changes in synapse morphology and function. A recent Nature Neuroscience paper reports a new post-translational modification that is required to coordinate



the changes involved in memory formation: after enhanced synaptic activity,DHHC5 palmitoylates δ-catenin, increasing its binding to synaptic cadherin both in vitro and in the hippocampus of fear-conditioned rodents.


These researchers used a synthetic δ-catenin gene, in which the palmitoylated cysteine residues were mutated to serine, to demonstrate that δ-catenin palmitoylation is required for numerous facets of activity-induced synaptic plasticity, including N-cadherin stabilization at synapses, postsynaptic spine enlargement, insertion of GluA1 and GluA2 into the synaptic membrane, and increased mEPSC amplitude.


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