Differential role of CaMK in synaptic tagging and capture

Long-term potentiation (LTP) of synaptic connectivity is theorized to be a physiological correlate of memory formation. Changes in synaptic strength, as well as their maintenance, depend on a network of chemical interactions that occur both locally at the synapse and across the dendrites, axons, and nucleus of the neuron. The Calmodulin Kinase (CaMK) family can be divided into CaMKI/IV and CaMKII subfamilies among others, all with central roles in synaptic plasticity. The question that we address in this chapter is whether the necessary roles of particular CaM Kinases in LTP are restricted to the synthesis of plasticity-related products or to the local phosphorylation of synaptic proteins. We use analytically powerful three-pathway protocols and kinase-specifi c drugs to dissociate the distinct roles of the CaMK pathways in LTP.