Depolarization drives β-catenin into neuronal spines promoting changes in synaptic structure and function

Sachiko Murase, Eric Mosser, Erin M. Schuman

Research output: Contribution to journalArticlepeer-review

288 Scopus citations

Abstract

Activity-induced changes in adhesion molecules may coordinate presynaptic and postsynaptic plasticity. Here, we demonstrate that β-catenin, which mediates interactions between cadherins and the actin cytoskeleton, moves from dendritic shafts into spines upon depolarization, increasing its association with cadherins. β-catenin's redistribution was mimicked or prevented by a tyrosine kinase or phosphatase inhibitor, respectively. Point mutations of β-catenin's tyrosine 654 altered the shaft/spine distribution: Y654F-β-catenin-GFP (phosphorylation-prevented) was concentrated in spines, whereas Y654E-β-catenin-GFP (phosphorylation-mimic) accumulated in dendritic shafts. In Y654F-expressing neurons, the PSD-95 or associated synapsin-I clusters were larger than those observed in either wild-type-β-catenin or also Y654E-expressing neurons. Y654F-expressing neurons exhibited a higher minifrequency. Thus, neural activity induces β-catenin's redistribution into spines, where it interacts with cadherin to influence synaptic size and strength.

Original languageEnglish (US)
Pages (from-to)91-105
Number of pages15
JournalNeuron
Volume35
Issue number1
DOIs
StatePublished - Jul 3 2002

ASJC Scopus subject areas

  • Neuroscience(all)

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