Evidence map›Paper›PMID 37650965›Full record

ArticleMolecular neurobiology2024

Inversed Effects of Nav1.2 Deficiency at Medial Prefrontal Cortex and Ventral Tegmental Area for Prepulse Inhibition in Acoustic Startle Response.

Toshimitsu Suzuki, Satoko Hattori, Hiroaki Mizukami, Ryuichi Nakajima, Yurina Hibi, Saho Kato, Mahoro Matsuzaki, Ryu Ikebe, Tsuyoshi Miyakawa, Kazuhiro Yamakawa

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Article
  3. DecipheringArXiv · 2024
    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

10 authors at 3 institutions in 1 country.

Toshimitsu SuzukiDepartment of Neurodevelopmental Disorder Genetics, Institute of Brain Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi, 467-8601, Japan. toshi@med.nagoya-cu.ac.jp.ORCID http://orcid.org/0000-0003-0585-5692
Satoko HattoriDivision of Systems Medical Science, Center for Medical Science, Fujita Health University, Toyoake, Aichi, 470-1192, Japan.ORCID http://orcid.org/0000-0002-1047-6454
Hiroaki MizukamiDivision of Genetic Therapeutics, Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Tochigi, 329-0498, Japan.ORCID http://orcid.org/0000-0001-8954-874X
Ryuichi NakajimaDivision of Systems Medical Science, Center for Medical Science, Fujita Health University, Toyoake, Aichi, 470-1192, Japan.ORCID http://orcid.org/0000-0002-0024-4422
Yurina HibiDepartment of Neurodevelopmental Disorder Genetics, Institute of Brain Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi, 467-8601, Japan.
Saho KatoDepartment of Neurodevelopmental Disorder Genetics, Institute of Brain Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi, 467-8601, Japan.
Mahoro MatsuzakiDepartment of Neurodevelopmental Disorder Genetics, Institute of Brain Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi, 467-8601, Japan.
Ryu IkebeDepartment of Neurodevelopmental Disorder Genetics, Institute of Brain Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi, 467-8601, Japan.
Tsuyoshi MiyakawaDivision of Systems Medical Science, Center for Medical Science, Fujita Health University, Toyoake, Aichi, 470-1192, Japan.ORCID http://orcid.org/0000-0003-0137-8200
Kazuhiro YamakawaDepartment of Neurodevelopmental Disorder Genetics, Institute of Brain Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi, 467-8601, Japan.ORCID http://orcid.org/0000-0002-1478-4390
Nagoya City University · JPFujita Health University · JPJichi Medical University · JP

Funding

AMED JP19dm0107101JSPS KAKENHI 16H06276 (AdAMS)JSPS KAKENHI JP 20H03566JSPS KAKENHI JP 22H04922 (AdAMS)JSPS KAKENHI JP 22K07620MEXT Promotion of Distinctive Joint Research Center Program JPMXP0621467949
6 · The paper itself

Abstract

Numerous pathogenic variants of SCN2A gene, encoding voltage-gated sodium channel α2 subunit Nav1.2 protein, have been identified in a wide spectrum of neuropsychiatric disorders including schizophrenia. However, pathological mechanisms for the schizophrenia-relevant behavioral abnormalities caused by the variants remain poorly understood. Here in this study, we characterized mouse lines with selective Scn2a deletion at schizophrenia-related brain regions, medial prefrontal cortex (mPFC) or ventral tegmental area (VTA), obtained by injecting adeno-associated viruses (AAV) expressing Cre recombinase into homozygous Scn2a-floxed (Scn2a

Indexed as

Prepulse InhibitionReflex, StartleAcousticsAnimalsHumansMicePrefrontal CortexVentral Tegmental AreamPFCNAcNav1.2SchizophreniaScn2a

Identifiers

PMID37650965
OpenAlexW4386306134

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.