Evidence map›Paper›PMID 23497716›Full record

ArticleMolecular brain2013

Synaptosomal-associated protein 25 mutation induces immaturity of the dentate granule cells of adult mice.

Koji Ohira, Katsunori Kobayashi, Keiko Toyama, Hironori K Nakamura, Hirotaka Shoji, Keizo Takao, Rika Takeuchi, Shun Yamaguchi, Masakazu Kataoka, Shintaro Otsuka and 2 more

Open access · goldAbstract read
In one paragraph

Article in Molecular brain, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 5% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
  2. Hyper-maturity and accelerated aging in the hippocampus of mouse models of neuropsychiatric disorders with anxiety-like behavior.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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  9. Adult neural stem cells and schizophrenia.World journal of stem cells · 2022
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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

12 authors at 5 institutions in 1 country.

Koji OhiraDivision of Systems Medical Science, Institute for Comprehensive Medical Science, Fujita Health University, Toyoake, 470-1192, Japan.
Katsunori Kobayashi
Keiko Toyama
Hironori K Nakamura
Hirotaka Shoji
Keizo Takao
Rika Takeuchi
Shun Yamaguchi
Masakazu Kataoka
Shintaro Otsuka
Masami Takahashi
Tsuyoshi Miyakawa
Japan Science and Technology Agency · JPFujita Health University · JPKitasato University · JPNational Institute for Physiological Sciences · JPShinshu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSynaptosomal-associated protein, 25 kDa (SNAP-25) regulates the exocytosis of neurotransmitters. Growing evidence suggests that SNAP-25 is involved in neuropsychiatric disorders, such as schizophrenia, attention-deficit/hyperactivity disorder, and epilepsy. Recently, increases in anxiety-related behaviors and epilepsy have been observed in SNAP-25 knock-in (KI) mice, which have a single amino acid substitution of Ala for Ser187. However, the molecular and cellular mechanisms underlying the abnormalities in this mutant remain unknown.

resultsIn this study, we found that a significant number of dentate gyrus (DG) granule cells was histologically and electrophysiologically similar to immature DG neurons in the dentate gyrus of the adult mutants, a phenomenon termed the "immature DG" (iDG). SNAP-25 KI mice and other mice possessing the iDG phenotype, i.e., alpha-calcium/calmodulin-dependent protein kinase II heterozygous mice, Schnurri-2 knockout mice, and mice treated with the antidepressant fluoxetine, showed similar molecular expression patterns, with over 100 genes similarly altered. A working memory deficit was also identified in mutant mice during a spontaneous forced alternation task using a modified T-maze, a behavioral task known to be dependent on hippocampal function. Chronic treatments with the antiepileptic drug valproate abolished the iDG phenotype and the working memory deficit in mutants.

conclusionsThese findings suggest that the substitution of Ala for Ser187 in SNAP-25 induces the iDG phenotype, which can also be caused by epilepsy, and led to a severe working memory deficit. In addition, the iDG phenotype in adulthood is likely an endophenotype for at least a part of some common psychiatric disorders.

Indexed as

AgingAnimalsBiomarkersCytoskeletal ProteinsDentate GyrusGene Expression ProfilingGene Knock-In TechniquesMemory, Short-TermMiceMice, Mutant StrainsMutationNerve Tissue ProteinsNeurogenesisPhenotypePromoter Regions, GeneticSynaptosomal-Associated Protein 25activity regulated cytoskeletal-associated proteinBiomarkersCytoskeletal ProteinsNerve Tissue ProteinsSnap25 protein, mouseSynaptosomal-Associated Protein 25Valproic Acid

Identifiers

PMID23497716
PMCPMC3605216
OpenAlexW2120257505

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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.