Memory reconsolidation is the process in which reactivated long-term memory (LTM) becomes transiently sensitive to amnesic agents that are effective at consolidation. The phenomenon was first described more than 50 years ago but did not fit the dominant paradigm that posited that consolidation takes place only once per LTM item. Reconsolidation was revitalized a decade ago using auditory fear conditioning in the rat and was shown to involve neural circuitry in the basolateral amygdala. Since then, reconsolidation has been demonstrated with many species, tasks, and amnesic agents, and cellular and molecular correlates of reconsolidation have been identified. I will discuss the evidence on which reconsolidation is based, and why specific impairments in consolidation, reconsolidation and LTM maintenance always lead to memory erasure.
I will also refer to potential clinical implications of reconsolidation. These include the ability to cause the synaptic circuit manifestations of a variety of psychopathologies to become transiently un-stored. If the mechanisms mediating restabilization of these circuit changes are prevented by behavioral or pharmacological intervention, an individual’s psychopathology could be reduced within a single session. This approach has been shown to work for PTSD, drug-cue induced craving, and Phobias.