β-catenin is required for memory consolidation

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Abstract
Structural changes in the dendrites are mediated in part by a cell adhesion molecule, β-catenin, and are associated with memory formation and maintenance. A new study by Maguschak and Ressler shows that β-catenin has a selective role in fear memory consolidation. β-catenin has been implicated in neuronal synapse regulation and remodeling. Here we have examined β-catenin expression in the adult mouse brain and its role in amygdala-dependent learning and memory. We found alterations in β-catenin mRNA and protein phosphorylation during fear-memory consolidation. Such alterations correlated with a change in the association of β-catenin with cadherin. Pharmacologically, this consolidation was enhanced by lithium-mediated facilitation of β-catenin. Genetically, the role of β-catenin was confirmed with site-specific deletions of loxP-flanked Ctnnb1 (encoding β-catenin) in the amygdala. Baseline locomotion, anxiety-related behaviors and acquisition or expression of conditioned fear were normal. However, amygdala-specific deletion of Ctnnb1 prevented the normal transfer of newly formed fear learning into long-term memory. Thus, β-catenin may be required in the amygdala for the normal consolidation, but not acquisition, of fear memory. This suggests a general role for β-catenin in the synaptic remodeling and stabilization underlying long-term memory in adults.