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Cadherins/metabolism
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Cytoskeletal Proteins/drug effects/genetics/*metabolism
Dendrites/drug effects/*metabolism/ultrastructure
Disks Large Homolog 4 Protein
Enzyme Inhibitors/pharmacology
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Hippocampus/cytology/*growth & development/*metabolism
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Neuronal Plasticity/drug effects/*genetics
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Protein-Tyrosine Kinases/antagonists & inhibitors/metabolism
Pyridinium Compounds
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Synapses/drug effects/*metabolism/ultrastructure
Synapsins/metabolism
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*Trans-Activators
Tyrosine/genetics/metabolism
beta Catenin
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.