Journal
CELL DEATH AND DIFFERENTIATION
Volume 22, Issue 9, Pages 1425-1436Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/cdd.2014.227
Keywords
-
Categories
Funding
- European Union [HEALTH-F2-2009-241498]
- BMBF [ERA-Net Neuron II CIPRESS]
- Italian Ministry of Health [RF-2009-1545998, RF-2009-1471694]
- PRIN
- Cariplo [2011-0540]
- Regione Lombardia Project MbMM-convenzione [18099/RCC]
- CNR Research Project on Aging
Ask authors/readers for more resources
Impairment of synaptic function can lead to neuropsychiatric disorders collectively referred to as synaptopathies. The SNARE protein SNAP-25 is implicated in several brain pathologies and, indeed, brain areas of psychiatric patients often display reduced SNAP-25 expression. It has been recently found that acute downregulation of SNAP-25 in brain slices impairs long-term potentiation; however, the processes through which this occurs are still poorly defined. We show that in vivo acute downregulation of SNAP-25 in CA1 hippocampal region affects spine number. Consistently, hippocampal neurons from SNAP-25 heterozygous mice show reduced densities of dendritic spines and defective PSD-95 dynamics. Finally, we show that, in brain, SNAP-25 is part of a molecular complex including PSD-95 and p140Cap, with p140Cap being capable to bind to both SNAP-25 and PSD-95. These data demonstrate an unexpected role of SNAP-25 in controlling PSD-95 clustering and open the possibility that genetic reductions of the protein levels - as occurring in schizophrenia - may contribute to the pathology through an effect on postsynaptic function and plasticity.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available