Fossati, G., Morini, R., Corradini, I., Antonucci, F., Trepte, P., Edry, E., Sharma, V., Papale, Alessandro ![]() ![]() |
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Abstract
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.
Item Type: | Article |
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Date Type: | Publication |
Status: | Published |
Schools: | Biosciences |
Additional Information: | Advance online publication 13 February 2015 PDF uploaded in accordance with publisher's policies at http://www.sherpa.ac.uk/romeo/issn/1350-9047/ (accessed 13/11/15). |
Publisher: | Nature Publishing Group |
ISSN: | 1350-9047 |
Date of First Compliant Deposit: | 30 March 2016 |
Date of Acceptance: | 26 November 2014 |
Last Modified: | 05 May 2023 18:27 |
URI: | https://orca.cardiff.ac.uk/id/eprint/76271 |
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