Evidence map›Paper›PMID 42844949›Full record

ArticleThe journal of gene medicine2026

Adeno-Associated Virus Vector-Mediated Expression of Neuroligin 2 in the Mouse Hippocampus Attenuates the Progression of Pentylenetetrazol-Induced Seizures.

Tomohiro Tokutake, Akane Hara, Ayano Murayama, Yuto Mitsuda, Jun Yokose, Yusuke Yano, Yuki Shigetsura, Mika Ito, Naomi Takino, Shinichi Kumagai and 3 more

Abstract read
In one paragraph

Article in The journal of gene medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Tomohiro TokutakeDepartment of Pharmaceutical Therapy & Neuropharmacology, Faculty of Pharmaceutical Sciences, University of Toyama, Toyama, Japan.
Akane HaraLaboratory of Mathematical Medicine and Pharmaceutical Assessment, Faculty of Pharmaceutical Sciences, University of Toyama, Toyama, Japan.ORCID https://orcid.org/0000-0003-2483-6489
Ayano MurayamaDepartment of Pharmaceutical Therapy & Neuropharmacology, Faculty of Pharmaceutical Sciences, University of Toyama, Toyama, Japan.
Yuto MitsudaDepartment of Pharmaceutical Therapy & Neuropharmacology, Faculty of Pharmaceutical Sciences, University of Toyama, Toyama, Japan.
Jun YokoseDepartment of Pharmaceutical Therapy & Neuropharmacology, Faculty of Pharmaceutical Sciences, University of Toyama, Toyama, Japan.ORCID https://orcid.org/0000-0002-1953-9378
Yusuke YanoDepartment of Pharmaceutical Therapy & Neuropharmacology, Faculty of Pharmaceutical Sciences, University of Toyama, Toyama, Japan.ORCID https://orcid.org/0009-0006-1231-0649
Yuki ShigetsuraDepartment of Clinical Pharmacology and Therapeutics, Kyoto University Hospital, Kyoto, Japan.ORCID https://orcid.org/0000-0001-7033-5357
Mika ItoDivision of Neurological Gene Therapy, Center for Open Innovation, Jichi Medical University, Shimotsuke, Japan.
Naomi TakinoDivision of Neurological Gene Therapy, Center for Open Innovation, Jichi Medical University, Shimotsuke, Japan.
Shinichi KumagaiDepartment of Neurosurgery, Jichi Medical University, Shimotsuke, Japan.
Kuniko ShimazakiDepartment of Neurosurgery, Jichi Medical University, Shimotsuke, Japan.
Shin-Ichi MuramatsuDivision of Neurological Gene Therapy, Center for Open Innovation, Jichi Medical University, Shimotsuke, Japan.ORCID https://orcid.org/0000-0002-3185-7790
Atsumi NittaDepartment of Pharmaceutical Therapy & Neuropharmacology, Faculty of Pharmaceutical Sciences, University of Toyama, Toyama, Japan.ORCID https://orcid.org/0000-0001-6916-9160

Funding

Japan Agency for Medical Research and Development JP25bk0104166Japan Society for the Promotion of Science JP21H02632Japan Society for the Promotion of Science JP22H04922JST SPRING JPMJSP2145SRF Grant for Biomedical Research and FoundationTamura Foundation
6 · The paper itself

Abstract

Gene therapy can target specific brain regions and may be an effective therapeutic tool for drug-resistant epilepsy. Neuroligin 2 (NL2) is a postsynaptic cell-adhesion protein involved in the formation of inhibitory synapses. Since epileptic seizures are attributed to excessive brain neuronal activity, we hypothesized that NL2-mediated inhibitory signaling suppresses seizures. Male C57BL/6J mice were bilaterally injected into the hippocampus (HPC) with an adeno-associated virus (AAV) vector expressing NL2 under the control of synapsin I promoter (AAV-NL2). Mice treated with AAV-NL2 were intraperitoneally administered with 35 mg/kg pentylenetetrazol (PTZ) every other day. Ordinal logistic regression analysis revealed that NL2 expression exerted a protective effect against seizure progression induced by repeated PTZ administration. In addition, ventral HPC c-Fos protein levels were significantly suppressed with AAV-NL2 injection. NL2 expression induced by intra-HPC AAV-NL2 injection attenuates the progression of PTZ-induced seizures and may represent a potential target for seizure control.

Indexed as

Cell Adhesion Molecules, NeuronalDependovirusGenetic VectorsHippocampusNeuroliginsSeizuresAnimalsDisease Models, AnimalDisease ProgressionGene ExpressionGenetic TherapyMaleMiceMice, Inbred C57BLNerve Tissue ProteinsPentylenetetrazoleCell Adhesion Molecules, NeuronalNerve Tissue Proteinsneuroligin 2NeuroliginsPentylenetetrazoleProto-Oncogene Proteins c-fosadeno‐associated virusepilepsyhippocampusneuroligin 2pentylenetetrazolseizure

Identifiers

PMID42844949
PMCPMC13646667

What OpenQuestion holds

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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.