The main cellular mechanisms underlying memory formation are protein synthesis-dependent forms of long-term potentiation (late-LTP) and long-term depression (late-LTD). Recent data support the hypothesis that neurons store relevant information by processes of ‘synaptic tagging’ in dendritic, functional compartments during late-LTP and late-LTD, rather than in single synapses. Plasticity-related proteins (PRPs), partially non-specific to the locally induced process are synthesized in dendritic compartments and then captured by local, process-specific synaptic tags. We support these findings in two ways 1) late-LTP/LTD, locally induced in apical or basal dendrites of hippocampal CA1 neurons, normally does not spread to the basal or apical compartment, respectively; 2) the specificity of the synaptic plasticity event is achieved by the activation of process- and compartment-specific synaptic tag molecules. We have identified CaMKII as the first LTP-specific, and ERK1/2 as LTD-specific tag molecules in apical dendritic CA1-compartments, while PKA and PKMζ jointly mediate LTP-specific tags in basal dendrites. Under distinct circumstances however, functional compartmentalization can be overwritten by behavioral acts representing specific information. I will present findings supporting this hypothesis.