Targeted pharmacological or behavioural interventions applied at the time of retrieval of an emotional memory can persistently block its later expression, perhaps due to memory erasure. The possibility to block the expression of targeted emotional memories carries enormous potential for the treatment of emotional memory disorders such as anxiety, depression, PTSD and addiction. In the current project, we explored the nature of such post-reminder amnesia and the conditions under which it occurs. In particular, we wanted to uncover whether post-reminder amnesia reflects memory erasure (a storage or retention deficit) or an impairment to retrieve an otherwise intact memory trace (an expression or retrieval deficit), develop new techniques to block the expression of emotional meories, and reveal under which circumstances memories become sensitive to such amnestic interventions.
While we obtained evidence that the brain mechanisms underlying post-reminder amnesia may be partly different than those underlying other forms of memory suppression, we also found that post-reminder amnesia can be reversed if the reminder cues used for retrieval prior to the amnestic intervention are slightly dissimilar from cues present at the time of memory encoding. This suggests that post-reminder amnesia does not need to result from memory erasure but may merely reflect impaired memory retrieval. Moreover, we found that both pharmacologically induced and other documented forms of post-reminder amnesia are often not readily replicable, for reasons that are only partially understood, and that the literature on this topic suffers from considerable publication bias. In combination with the observation that post-reminder amnesia is reversible, this suggests that the existing literature paints an overly optimistic picture of the potential for clinical translation.
