Maladaptive fears are often treated using therapies based on extinction—re-exposure to a feared stimulus in a safe environment. Although these treatments can be effective, relapse is common [1]. Since the time of Pavlov, relapse has been thought to indicate that extinction is new learning, not unlearning [2]. From this perspective, relapse is a mnemonic phenomenon in which two opposing memory traces vie for expression. Recent work suggests that the hippocampus is an arena in which this competition plays out.

Experiments in mice demonstrate that the hippocampal dentate gyrus (DG) generates a contextual fear “engram.” Immediate-early gene-based tagging of neurons active during acquisition of contextual fear—fear of the chamber in which a footshock was given—shows that these neurons are reactivated during recall of contextual fear [3]. Furthermore, optogenetic experiments demonstrate that this reactivation is necessary and sufficient for expression of contextual fear [3, 4]. Two recent studies investigated what happens to hippocampal fear ensembles when contextual fear is extinguished.

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