Memory Destabilization and Reconsolidation Dynamically Regulate the PKMξ Maintenance Mechanism

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

Automated summary

The study found that NMDAR activation and proteasome activity can lead to a temporary reduction in PKM xi protein after memory retrieval, while new PKM xi protein is synthesized during memory reconsolidation to restore memory. Failure to synthesize new PKM xi during memory reconsolidation impairs memory, but continuous synthesis of PKM xi is not necessary for maintenance itself.