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Reduced SNAP-25 increases PSD-95 mobility and impairs spine morphogenesis.

G Fossati1, R Morini1, I Corradini2

  • 11] Department of Biotechnology and Translational Medicine, University of Milan, Milano 20129, Italy [2] Humanitas Clinical and Research Center, Laboratory of Pharmacology and Brain Pathology, Via Manzoni 56, Rozzano, 20089 Milano, Italy.

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Summary
This summary is machine-generated.

Reduced SNAP-25 protein levels impair synaptic function and may contribute to neuropsychiatric disorders like schizophrenia by affecting dendritic spine density and PSD-95 dynamics.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Synaptic Plasticity

Background:

  • Synaptic dysfunction underlies synaptopathies, a class of neuropsychiatric disorders.
  • Reduced SNAP-25 expression is observed in psychiatric patients' brain regions.
  • The precise mechanisms by which SNAP-25 impacts synaptic function are not fully understood.

Purpose of the Study:

  • To investigate the in vivo role of SNAP-25 in synaptic structure and function.
  • To elucidate the molecular interactions of SNAP-25 at the postsynaptic level.
  • To explore the potential contribution of SNAP-25 reduction to psychiatric pathologies.

Main Methods:

  • In vivo acute downregulation of SNAP-25 in the CA1 hippocampal region.
  • Analysis of dendritic spine number and density in hippocampal neurons.
  • Assessment of PSD-95 dynamics in SNAP-25 heterozygous mouse neurons.
  • Co-immunoprecipitation to identify SNAP-25 interacting proteins.

Main Results:

  • Acute SNAP-25 downregulation in vivo affects hippocampal spine number.
  • SNAP-25 heterozygous mice exhibit reduced dendritic spine density and impaired PSD-95 dynamics.
  • SNAP-25 forms a molecular complex with PSD-95 and p140Cap in the brain.
  • p140Cap binds to both SNAP-25 and PSD-95.

Conclusions:

  • SNAP-25 plays a critical role in regulating PSD-95 clustering and postsynaptic function.
  • Reduced SNAP-25 levels, as seen in schizophrenia, may impair synaptic plasticity.
  • These findings suggest a novel mechanism linking SNAP-25 deficiency to synaptopathies.