The Neural Mechanisms Underlying Memory Formation

Trying to forget the past may inadvertently cause amnesia for the present. This surprising possibility follows from the neural mechanisms underlying memory formation and motivated forgetting. Decades of research on memory formation show that the hippocampus is essential for constructing new episodic memories. Hippocampal damage irreversibly harms people’s ability to store new memories, causing profound amnesia for life’s events1,2. Reversibly disturbing the hippocampus through optogenetic, electrical and pharmacological interventions temporarily disrupts memory formation3,4. Research on motivated forgetting, on the other hand, indicates that people often downregulate hippocampal activity through cognitive control when they are reminded of†¦show more content†¦1). In the TNT procedure, people perform trials requiring them to attend to a reminder of a past event; for each reminder, they are cued to retrieve the associated memory (Think trials), or to suppress its retrieval (No-Think trials). Suppressing retrieval in response to a strong reminder reduces blood–oxygen-level dependent activation in the hippocampus and impairs retention of the suppressed memory5–11. These reductions originate from inhibitory control processes supported by the dorsolateral prefrontal cortex6–11. Retrieving memories, in contrast, increases hippocampal activity12 and often facilitates later recall13. Thus, hippocampal activity can be modulated according to task goals, though practice at suppressing retrieval is often necessary to achieve hippocampal reductions6. A key assumption of the present work is that this modulation does not target particular memories, which may be a person’s goal, but rather reflects a broadly targeted suppression (h ereinafter, ‘systemic suppression’) of regional activity in the hippocampus that generally disrupts other memory functions supported by this region. For instance, beyond simply disrupting episodic retrieval, systemically suppressing hippocampal activity may also prevent freshly encoded stimulus input from generating new hippocampal traces