Memory destabilization and reconsolidation dynamically regulate the PKMζ maintenance mechanism
Useful memory must balance between stability and malleability. This puts effective memory storage at odds with plasticity processes like reconsolidation. What becomes of memory maintenance processes during synaptic plasticity is unknown. Here we examined the fate of the memory maintenance protein PKM{zeta} during memory destabilization and reconsolidation. We found that NMDA receptor activation and proteasome activity induced a transient reduction in PKM{zeta} protein following retrieval. During reconsolidation, new PKM{zeta} was synthesized to re-store the memory. Failure to synthesize new PKM{zeta} during reconsolidation impaired memory but uninterrupted PKM{zeta} translation was not necessary for maintenance itself. Finally, NMDA receptor activation was necessary to render memories vulnerable to the amnesic effect of PKM{zeta}-antisense. These findings outline a transient collapse and renewal of the PKM{zeta} memory maintenance mechanism during plasticity. We argue that dynamic changes in PKM{zeta} protein levels can serve as an exemplary model of the molecular changes underlying memory destabilization and reconsolidation.