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Related Experiment Video

Updated: May 9, 2026

3D Modeling of Dendritic Spines with Synaptic Plasticity

3D Modeling of Dendritic Spines with Synaptic Plasticity

Published on: May 18, 2020

SNAP-25 regulates spine formation through postsynaptic binding to p140Cap.

Romana Tomasoni¹, Daniele Repetto, Raffaella Morini

¹Department of Biotechnology and Translational Medicine, University of Milan, V Vanvitelli 32, Milano 20129, Italy.

Nature Communications

|July 23, 2013

Summary

Synaptosomal-associated protein of 25 kDa (SNAP-25) regulates dendritic spine development. Reduced SNAP-25 leads to immature spines, while increased levels promote mature spine formation and function.

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3D Modeling of Dendritic Spines with Synaptic Plasticity

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Area of Science:

Neuroscience
Molecular Biology
Cell Biology

Background:

Synaptosomal-associated protein of 25 kDa (SNAP-25) is crucial for synaptic vesicle exocytosis and ion channel regulation.
The Soluble N-ethylmaleimide-sensitive-factor attachment protein receptors (SNARE) family, including SNAP-25, plays vital roles in neuronal function.

Purpose of the Study:

To investigate the role of SNAP-25 in dendritic spine morphogenesis and function.
To elucidate the molecular mechanisms by which SNAP-25 influences spine development.

Main Methods:

Manipulating SNAP-25 expression levels in neurons.
Analyzing dendritic spine morphology and maturity using microscopy.
Assessing spine functionality and molecular composition.

Main Results:

Acute reduction of SNAP-25 expression resulted in immature and less functional dendritic spines.
Over-expression of SNAP-25 increased the density of mature, Postsynaptic Density protein 95 (PSD-95)-positive spines.
SNAP-25's regulation of spine morphogenesis involves binding to the plasma membrane and the p140Cap protein.

Conclusions:

SNAP-25 is a key regulator of dendritic spine maturation and function.
SNAP-25 facilitates spine formation by recruiting and stabilizing the actin-regulating protein p140Cap.