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Significance Within a restricted time window, a brief exposure to a novel environment enhances the extinction of contextual fear. This can be explained by a hippocampal process of behaviorally induced synaptic tagging and capture. Here, we report that the effect requires glutamate NMDA receptors and L-voltage–dependent calcium channels and involves the activation of calcium/calmodulin-dependent protein kinase II, in addition to both ribosomal and nonribosomal protein synthesis. All these mechanisms operate only when the proteasomal-ubiquitin protein degradation system is intact, which suggests that they depend on synaptic protein turnover. Extinction enhancement by novelty is of great potential importance in the treatment of fear memories, such as those of posttraumatic stress disorder; the treatments of choice for such conditions are based on extinction procedures.

Hippocampal molecular mechanisms involved in the enhancement of fear extinction caused by exposure to novelty