Molecular mechanisms controlling protein synthesis in memory reconsolidation.

It is currently well established that the synthesis of new proteins (mRNA translation) is required for long-lasting synaptic plasticity and memory formation. Translation in the brain is regulated primarily at the initiation stage by general as well as by gene-specific mechanisms. Stored memories can become sensitive to interference upon reactivation, through a process termed reconsolidation, which depends on protein synthesis. Here, I examine the role of translation control mechanisms, focusing particularly on the mechanistic target of rapamycin complex 1 (mTORC1), in reconsolidation.