Depolarization drives beta-Catenin into neuronal spines promoting changes in 
synaptic structure and function

Murase, S.; Mosser, E.; Schuman, Erin M.

doi:10.1016/s0896-6273(02)00764-x

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Journal Article

Depolarization drives beta-Catenin into neuronal spines promoting changes in synaptic structure and function

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Schuman, Erin M.
Synaptic Plasticity Department, Max Planck Institute for Brain Research, Max Planck Society;

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https://www.ncbi.nlm.nih.gov/pubmed/12123611
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Citation

Murase, S., Mosser, E., & Schuman, E. M. (2002). Depolarization drives beta-Catenin into neuronal spines promoting changes in synaptic structure and function. Neuron, 35(1), 91-105. doi:10.1016/s0896-6273(02)00764-x.

Cite as: https://hdl.handle.net/21.11116/0000-0007-EF7C-2

Abstract

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