Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

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

Sachiko Murase1, Eric Mosser, Erin M Schuman

  • 1Caltech/HHMI, Division of Biology, 216-76, 1200 East California Boulevard, Pasadena 91125, USA.

Neuron
|July 19, 2002
PubMed
Summary

Neural activity drives beta-catenin into dendritic spines, enhancing synaptic connections. This movement, regulated by phosphorylation, influences synaptic size and strength, crucial for brain plasticity.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

The Development of Immunological Quantification Method for Glycyrrhetinic Acid in Serum to Estimate the Potential Risk for Pseudoaldsteronism.

Planta medica·2026
Same author

Ribosomal RNA expansion segments mediate the oligomerization of inactive animal ribosomes.

Science (New York, N.Y.)·2026
Same author

An integrated transcriptomic and proteomic map of the mouse hippocampus at synaptic resolution.

Nature communications·2025
Same author

Cell type-specific in vivo proteomes with a multicopy mutant methionyl tRNA synthetase mouse line.

Lab animal·2025
Same author

Neuronal processes contain the essential components for the late steps of ribosome biogenesis.

Proceedings of the National Academy of Sciences of the United States of America·2025
Same author

Prolonged visual deprivation in adults induces non-homeostatic plasticity of feed-forward excitation from visual thalamus to cortex.

bioRxiv : the preprint server for biology·2024

Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • Synaptic plasticity underlies learning and memory.
  • Adhesion molecules play a role in coordinating synaptic function.
  • Beta-catenin links cadherins to the cytoskeleton, influencing cell adhesion and signaling.

Purpose of the Study:

  • To investigate the role of beta-catenin in activity-induced synaptic plasticity.
  • To determine how beta-catenin's localization and phosphorylation affect synaptic structure and function.

Main Methods:

  • Utilized live-cell imaging and Förster resonance energy transfer (FRET) to track beta-catenin dynamics in neurons.
  • Employed pharmacological inhibitors of tyrosine kinases and phosphatases to modulate beta-catenin activity.
  • Introduced point mutations in beta-catenin (Y654F and Y654E) to mimic or prevent phosphorylation.

Related Experiment Videos

  • Assessed synaptic structure and function by quantifying postsynaptic density protein 95 (PSD-95) and synapsin-I clusters and measuring miniature synaptic event frequency.

    • Main Results:

    • Neural depolarization induced beta-catenin redistribution from dendritic shafts to spines, increasing its association with cadherins.
    • Tyrosine kinase inhibitors mimicked this redistribution, while phosphatase inhibitors prevented it.
    • The Y654F mutation (phosphorylation-prevented) led to spine concentration of beta-catenin, while Y654E (phosphorylation-mimic) resulted in shaft accumulation.
    • Neurons expressing Y654F-beta-catenin showed larger PSD-95/synapsin-I clusters and increased miniature event frequency compared to wild-type or Y654E.

    Conclusions:

    • Neural activity triggers beta-catenin's translocation into dendritic spines.
    • Beta-catenin phosphorylation at tyrosine 654 is a key regulatory mechanism for its activity-dependent localization.
    • Beta-catenin's spine localization is essential for modulating synaptic size and strength, contributing to synaptic plasticity.