Evidence map›Paper›PMID 29318050›Full record

ArticleNeural plasticity2017

Brain-Specific SNAP-25 Deletion Leads to Elevated Extracellular Glutamate Level and Schizophrenia-Like Behavior in Mice.

Hua Yang, Mengjie Zhang, Jiahao Shi, Yunhe Zhou, Zhipeng Wan, Yicheng Wang, Yinghan Wan, Jun Li, Zhugang Wang, Jian Fei

Open access · goldAbstract read
In one paragraph

Article in Neural plasticity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
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  11. Dynamic Changes of Brain Cilia Transcriptomes across the Human Lifespan.International journal of molecular sciences · 2021
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  14. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021
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  18. Post-mortem Characterisation of a Case With anFrontiers in physiology · 2019
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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

10 authors at 2 institutions in 1 country.

Hua YangSchool of Life Science and Technology, Tongji University, Shanghai 200092, China.
Mengjie ZhangSchool of Life Science and Technology, Tongji University, Shanghai 200092, China.
Jiahao ShiSchool of Life Science and Technology, Tongji University, Shanghai 200092, China.
Yunhe ZhouSchool of Life Science and Technology, Tongji University, Shanghai 200092, China.
Zhipeng WanSchool of Life Science and Technology, Tongji University, Shanghai 200092, China.
Yicheng WangShanghai Engineering Research Center of Model Organisms (SRCMO/SMOC), Shanghai 201203, China.
Yinghan WanShanghai Engineering Research Center of Model Organisms (SRCMO/SMOC), Shanghai 201203, China.
Jun LiShanghai Engineering Research Center of Model Organisms (SRCMO/SMOC), Shanghai 201203, China.
Zhugang WangShanghai Engineering Research Center of Model Organisms (SRCMO/SMOC), Shanghai 201203, China.
Jian FeiSchool of Life Science and Technology, Tongji University, Shanghai 200092, China.ORCID 0000-0001-7755-0818
Tongji University · CNShanghai Model Organisms (China) · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several studies have associated reduced expression of synaptosomal-associated protein of 25 kDa (SNAP-25) with schizophrenia, yet little is known about its role in the illness. In this paper, a forebrain glutamatergic neuron-specific SNAP-25 knockout mouse model was constructed and studied to explore the possible pathogenetic role of SNAP-25 in schizophrenia. We showed that SNAP-25 conditional knockout (cKO) mice exhibited typical schizophrenia-like phenotype. A significantly elevated extracellular glutamate level was detected in the cerebral cortex of the mouse model. Compared with Ctrls, SNAP-25 was dramatically reduced by about 60% both in cytoplasm and in membrane fractions of cerebral cortex of cKOs, while the other two core members of SNARE complex: Syntaxin-1 (increased ~80%) and Vamp2 (increased ~96%) were significantly increased in cell membrane part. Riluzole, a glutamate release inhibitor, significantly attenuated the locomotor hyperactivity deficits in cKO mice. Our findings provide

Indexed as

AnimalsBehavior, AnimalCerebral CortexGlutamic AcidMiceMice, KnockoutNeuronsSchizophreniaSynaptic TransmissionSynaptosomal-Associated Protein 25Syntaxin 1Vesicle-Associated Membrane Protein 2Glutamic AcidSnap25 protein, mouseSynaptosomal-Associated Protein 25Syntaxin 1Vesicle-Associated Membrane Protein 2vesicle-associated membrane protein 2, mouse

Identifiers

PMID29318050
PMCPMC5727794
OpenAlexW2768370745

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.