Long-term potentiation (LTP) of synaptic strength is a candidate mechanism for the persistent modification of neural circuits thought to underlie memory. The molecular mechanism maintaining LTP and thus storing the memory trace, however, has, until recently, been elusive. Whereas the induction of late-LTP had been extensively studied and is exceedingly complex, the maintenance of the potentiation has only now been elucidated and involves a simpler network of molecules driven by a single newly synthesized gene product— the constitutively active PKC isoform, PKMz. Disrupting the maintenance network by inhibiting PKM reverses established late-LTP and rapidly erases long-term memory stored in a variety of neural circuits. A simple model of this maintenance network at synapses may explain both memory persistence and erasure.