Evidence map›Paper›PMID 19571127›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009

Mice with altered myelin proteolipid protein gene expression display cognitive deficits accompanied by abnormal neuron-glia interactions and decreased conduction velocities.

Hisataka Tanaka, Jianmei Ma, Kenji F Tanaka, Keizo Takao, Munekazu Komada, Koichi Tanda, Ayaka Suzuki, Tomoko Ishibashi, Hiroko Baba, Tadashi Isa and 4 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.6field-weighted citation impact, top 12% 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

43 citing papers in PubMed, 74 citations in OpenAlex.

  1. Mice lacking two alleles of the schizophrenia risk geneFrontiers in cellular neuroscience · 2026
    Article
  2. Article
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  5. Heterogeneity and regulation of oligodendrocyte morphology.Frontiers in cell and developmental biology · 2022
    Review
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  7. Article
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  9. Article
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  12. R-Ras1 and R-Ras2 Are Essential for Oligodendrocyte Differentiation and Survival for Correct Myelination in the Central Nervous System.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  13. Article
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  17. The neurobiology of transition to psychosis: clearing the cache.Journal of psychiatry & neuroscience : JPN · 2017
    Article
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  19. Review
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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

14 authors at 7 institutions in 5 countries.

Hisataka TanakaDivision of Neurobiology and Bioinformatics, National Institute for Physiological Sciences, Okazaki, Aichi 444-8787, Japan.
Jianmei Ma
Kenji F Tanaka
Keizo Takao
Munekazu Komada
Koichi Tanda
Ayaka Suzuki
Tomoko Ishibashi
Hiroko Baba
Tadashi Isa
Ryuichi Shigemoto
Katsuhiko Ono
Tsuyoshi Miyakawa
Kazuhiro Ikenaka
National Institutes of Natural Sciences · JPTokyo University of Pharmacy and Life Sciences · JPDalian Medical University · CNFujita Health University · JPKyoto Prefectural University of Medicine · JPKyoto University · JPNational Institute for Physiological Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Conduction velocity (CV) of myelinated axons has been shown to be regulated by oligodendrocytes even after myelination has been completed. However, how myelinating oligodendrocytes regulate CV, and what the significance of this regulation is for normal brain function remain unknown. To address these questions, we analyzed a transgenic mouse line harboring extra copies of the myelin proteolipid protein 1 (plp1) gene (plp1(tg/-) mice) at 2 months of age. At this stage, the plp1(tg/-) mice have an unaffected myelin structure with a normally appearing ion channel distribution, but the CV in all axonal tracts tested in the CNS is greatly reduced. We also found decreased axonal diameters and slightly abnormal paranodal structures, both of which can be a cause for the reduced CV. Interestingly the plp1(tg/-) mice showed altered anxiety-like behaviors, reduced prepulse inhibitions, spatial learning deficits and working memory deficit, all of which are schizophrenia-related behaviors. Our results implicate that abnormalities in the neuron-glia interactions at the paranodal junctions can result in reduced CV in the CNS, which then induces behavioral abnormalities related to schizophrenia.

Indexed as

Cognition DisordersGene Expression RegulationAdaptation, PsychologicalAnalysis of VarianceAnimalsAxonsCentral Nervous SystemExploratory BehaviorHand StrengthInhibition, PsychologicalKv1.2 Potassium ChannelMaze LearningMiceMice, Inbred StrainsMice, TransgenicMicroscopy, Electron, TransmissionKv1.2 Potassium ChannelMyelin Proteolipid ProteinPlp1 protein, mouse

Identifiers

PMID19571127
PMCPMC6665647
OpenAlexW1977061417

What OpenQuestion holds

Textmetadata
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.