The late temporal component of long-term potentiation (LTP), a putative neural mechanism for information storage in the brain, is protein synthesis-dependent, but the site of obligatory protein synthesis is not known. Here we show that when the protein synthesis inhibitor emetine is applied locally to the apical dendritic field of CA1 pyramidal cells in the murine hippocampus, late LTP is impaired at apical but not at basal dendrites, and conversely when emetine is applied locally to basal dendrites, late LTP is impaired only at basal dendrites. Thus, local protein synthesis modulates the expression of tetanically induced late LTP at Schaffer-commissural synapses on CA1 pyramidal cells.