Reconsolidation

Reconsolidation is the process by which a retrieved memory becomes destabilized and then restabilized through protein synthesis-dependent mechanisms, allowing modification before it is stored again. It is distinct from initial consolidation, which stabilizes a newly formed memory. Retrieval-induced lability means memories can be updated, strengthened, or weakened after retrieval.

Neural substrates include the hippocampus for contextual and relational aspects, the amygdala for emotional memories, and the prefrontal cortex for control and evaluation. Molecularly, reconsolidation requires protein synthesis, NMDA receptor signaling, and intracellular cascades such as CaMKII and CREB. Destabilization followed by restabilization involves protein turnover and synaptic remodeling. The destabilization window after retrieval typically lasts a few hours.

Whether reconsolidation occurs depends on boundary conditions such as prediction error, memory age, and retrieval context. Stronger or more entrenched memories may be less susceptible, while novelty and arousal can influence updating.

Clinically, reconsolidation has been explored as a way to modify fear, trauma, and addictive memories. Interventions include pharmacological disruption during retrieval, such as beta-adrenergic blockers like propranolol, and behavioral approaches like retrieval-extinction. The evidence is mixed, with variability across memory types and individuals, and further research is needed to establish safety, efficacy, and practical guidelines.