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Updated: May 26, 2026

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Rapid Golgi Stain for Dendritic Spine Visualization in Hippocampus and Prefrontal Cortex
Published on: December 3, 2021
Afadin, a Ras/Rap effector that controls cadherin function, promotes spine and excitatory synapse density in the
Gerard M J Beaudoin1, Claude M Schofield, Tulip Nuwal
1Department of Physiology, University of California, San Francisco, San Francisco, California 94158, USA.
Summary
Afadin is crucial for building synapses. Deleting afadin in neurons significantly reduced synapse formation and density, highlighting its essential role in brain development.
Area of Science:
- Neuroscience
- Molecular Biology
- Cell Biology
Background:
- Synaptogenesis, the formation of synapses, is vital for neural circuit development but its intracellular regulation is not fully understood.
- Afadin, an actin-binding protein, is known to regulate cell adhesion molecules and receptors, suggesting a role in synapse formation.
Purpose of the Study:
- To investigate the role of afadin in mediating synaptogenesis in the central nervous system.
- To determine the necessity of afadin for cadherin recruitment and synapse development in hippocampal neurons.
Main Methods:
- Conditional deletion of the afadin (mllt1) gene in postmitotic hippocampal neurons.
- Quantification of N-cadherin, β-catenin, αN-catenin, and EphB2 puncta densities.
- Assessment of spine and excitatory synapse densities using morphological analysis, marker apposition, and synaptic transmission measurements.
Main Results:
- Afadin deletion led to a 70% reduction in N-cadherin puncta and decreased densities of β-catenin, αN-catenin, and EphB2.
- A 40% decrease in spine and excitatory synapse densities was observed in the CA1 region.
- The remaining synapses showed normal function despite the reduced density.
Conclusions:
- Afadin is a key intracellular signaling molecule essential for cadherin recruitment during synaptogenesis.
- Afadin is necessary for the in vivo formation of spines and excitatory synapses in the hippocampus.
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