Evidence map›Paper›PMID 24409129›Full record

ArticleFrontiers in behavioral neuroscience2013

Mice lacking collapsin response mediator protein 1 manifest hyperactivity, impaired learning and memory, and impaired prepulse inhibition.

Naoya Yamashita, Aoi Takahashi, Keizo Takao, Toshifumi Yamamoto, Pappachan Kolattukudy, Tsuyoshi Miyakawa, Yoshio Goshima

Open access · goldAbstract read
In one paragraph

Article in Frontiers in behavioral neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Case report: AFrontiers in neuroscience · 2024
    Article
  3. Review
  4. MonoalleliceLife · 2022
    Article
  5. Article
  6. Article
  7. Article
  8. Clinical evidence that a dysregulated master neural network modulator may aid in diagnosing schizophrenia.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  9. Article
  10. Article
  11. International journal of molecular sciences · 2019
    Review
  12. Review
  13. Article
  14. Transcriptional regulation of CRMP5 controls neurite outgrowth through Sox5.Cellular and molecular life sciences : CMLS · 2018
    Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article
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

7 authors at 4 institutions in 2 countries.

Naoya YamashitaDepartment of Molecular Pharmacology and Neurobiology, Yokohama City University Graduate School of Medicine Yokohama, Japan.
Aoi TakahashiDepartment of Molecular Pharmacology and Neurobiology, Yokohama City University Graduate School of Medicine Yokohama, Japan.
Keizo TakaoSection of Behavior Patterns, Center for Genetic Analysis of Behavior, National Institute for Physiological Sciences Okazaki, Japan ; Genetic Engineering and Functional Genomics Group, Frontier Technology Center, Graduate School of Medicine, Kyoto University Kyoto, Japan ; Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency Kawaguchi, Japan.
Toshifumi YamamotoLaboratory of Molecular Psychopharmacology, Graduate School of Nanobiosciences, Yokohama City University Yokohama, Japan.
Pappachan KolattukudyBurnett School of Biomedical Sciences, College of Medicine, University of Central Florida Orlando, FL, USA.
Tsuyoshi MiyakawaSection of Behavior Patterns, Center for Genetic Analysis of Behavior, National Institute for Physiological Sciences Okazaki, Japan ; Genetic Engineering and Functional Genomics Group, Frontier Technology Center, Graduate School of Medicine, Kyoto University Kyoto, Japan ; Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency Kawaguchi, Japan ; Division of Systems Medical Science, Institute for Comprehensive Medical Science, Fujita Health University Toyoake, Japan.
Yoshio GoshimaDepartment of Molecular Pharmacology and Neurobiology, Yokohama City University Graduate School of Medicine Yokohama, Japan.
Yokohama City University · JPJapan Science and Technology Agency · JPKyoto University · JPUniversity of Central Florida · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Collapsin response mediator protein 1 (CRMP1) is one of the CRMP family members that are involved in various aspects of neuronal development such as axonal guidance and neuronal migration. Here we provide evidence that crmp1 (-/-) mice exhibited behavioral abnormalities related to schizophrenia. The crmp1 (-/-) mice exhibited hyperactivity and/or impaired emotional behavioral phenotype. These mice also exhibited impaired context-dependent memory and long-term memory retention. Furthermore, crmp1 (-/-) mice exhibited decreased prepulse inhibition, and this phenotype was rescued by administration of chlorpromazine, a typical antipsychotic drug. In addition, in vivo microdialysis revealed that the methamphetamine-induced release of dopamine in prefrontal cortex was exaggerated in crmp1 (-/-) mice, suggesting that enhanced mesocortical dopaminergic transmission contributes to their hyperactivity phenotype. These observations suggest that impairment of CRMP1 function may be involved in the pathogenesis of schizophrenia. We propose that crmp1 (-/-) mouse may model endophenotypes present in this neuropsychiatric disorder.

Indexed as

comprehensive behavioral testCRMP1hyperactivityknockout mousemesocortical dopaminergic transmissionprepulse inhibitionschizophrenia

Identifiers

PMID24409129
PMCPMC3873514
OpenAlexW2097057486

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.