Evidence map›Paper›PMID 25678324›Full record

ArticleCell death and differentiation2015

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

G Fossati, R Morini, I Corradini, F Antonucci, P Trepte, E Edry, V Sharma, A Papale, D Pozzi, P Defilippi and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors at 8 institutions in 3 countries.

G Fossati1] 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.
R Morini1] 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.
I Corradini1] Department of Biotechnology and Translational Medicine, University of Milan, Milano 20129, Italy [2] Istituto di Neuroscienze del CNR, Milano 20129, Italy.
F Antonucci1] Department of Biotechnology and Translational Medicine, University of Milan, Milano 20129, Italy [2] Istituto di Neuroscienze del CNR, Milano 20129, Italy.
P TrepteNeuroproteomics, Max Delbrueck Center for Molecular Medicine (MDC), Berlin 13125, Germany.
E EdrySagol Department of Neurobiology, Center for Gene Manipulation in the Adult Brain (CGMB), Haifa University, Haifa, Israel.
V SharmaSagol Department of Neurobiology, Center for Gene Manipulation in the Adult Brain (CGMB), Haifa University, Haifa, Israel.
A PapaleDivision of Neuroscience, Institute of Experimental Neurology, San Raffaele Scientific Institute and University, Milano 20132, Italy.
D PozziHumanitas Clinical and Research Center, Laboratory of Pharmacology and Brain Pathology, Via Manzoni 56, Rozzano, 20089 Milano, Italy.
P DefilippiDepartment of Molecular Biotechnology and Health Sciences, University of Torino, Torino 10124, Italy.
J C Meier1] RNA Editing and Hyperexcitability Disorders Helmholtz Group, Max Delbrück Center for Molecular Medicine, Berlin, Germany [2] TU Braunschweig, Zoological Institute, Division of Cell Biology and Cell Physiology, Braunschweig, Germany.
R BrambillaDivision of Neuroscience, Institute of Experimental Neurology, San Raffaele Scientific Institute and University, Milano 20132, Italy.
E TurcoDepartment of Molecular Biotechnology and Health Sciences, University of Torino, Torino 10124, Italy.
K RosenblumSagol Department of Neurobiology, Center for Gene Manipulation in the Adult Brain (CGMB), Haifa University, Haifa, Israel.
E E WankerNeuroproteomics, Max Delbrueck Center for Molecular Medicine (MDC), Berlin 13125, Germany.
N E ZivNetwork Biology Labs and Faculty of Medicine, Technion, 33000 Haifa, Israel.
E Menna1] Humanitas Clinical and Research Center, Laboratory of Pharmacology and Brain Pathology, Via Manzoni 56, Rozzano, 20089 Milano, Italy [2] Istituto di Neuroscienze del CNR, Milano 20129, Italy.
M Matteoli1] 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.
University of Milan · ITMax Delbrück Center · DEUniversity of Haifa · ILHumanitas University · ITNeuroscience Institute · ITUniversity of Turin · ITSan Raffaele University of Rome · ITTechnion – Israel Institute of Technology · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AnimalsDendritic SpinesDisks Large Homolog 4 ProteinGuanylate KinasesHEK293 CellsHippocampusHumansIntracellular Signaling Peptides and ProteinsMaleMembrane ProteinsMiceMice, Inbred C57BLMice, TransgenicMorphogenesisNeuronal PlasticitySynapsesDisks Large Homolog 4 ProteinDLG4 protein, humanDlg4 protein, mouseGuanylate KinasesIntracellular Signaling Peptides and ProteinsMembrane ProteinsSNAP25 protein, humanSnap25 protein, mouseSynaptosomal-Associated Protein 25

Identifiers

PMID25678324
PMCPMC4532770
OpenAlexW2094383620

What OpenQuestion holds

Textmetadata
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.