Evidence map›Paper›PMID 37774703›Full record

ArticleCell reports. Medicine2023

Shared GABA transmission pathology in dopamine agonist- and antagonist-induced dyskinesia.

Yoshifumi Abe, Sho Yagishita, Hiromi Sano, Yuki Sugiura, Masanori Dantsuji, Toru Suzuki, Ayako Mochizuki, Daisuke Yoshimaru, Junichi Hata, Mami Matsumoto and 9 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports. Medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

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  7. Morphological Changes in Direct Pathway Striatal Neurons in a Rat Model of Tardive Dyskinesia.Movement disorders : official journal of the Movement Disorder Society · 2026
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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

19 authors at 9 institutions in 2 countries.

Yoshifumi AbeDivision of Brain Sciences, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo 160-8582, Japan.
Sho YagishitaLaboratory of Structural Physiology, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, Tokyo 113-0033, Japan.
Hiromi SanoDivision of System Neurophysiology, National Institute for Physiological Sciences, 38 Nishigonaka, Myodaiji, Okazaki, Aichi 444-8585, Japan; Department of Physiological Sciences, SOKENDAI (The Graduate University for Advanced Studies), 38 Nishigonaka, Myodaiji, Okazaki, Aichi 444-8585, Japan; Division of Behavioral Pharmacology, International Center for Brain Science, Fujita Health University, 1-98 Dengakugakubo, Kutsukake-cho, Toyoake, Aichi 470-1192, Japan.
Yuki SugiuraDepartment of Biochemistry, Keio University School of Medicine, Tokyo 160-8582, Japan.
Masanori DantsujiDepartment of Oral Physiology, Showa University School of Dentistry, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.
Toru SuzukiDivision of Brain Sciences, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo 160-8582, Japan.
Ayako MochizukiDepartment of Oral Physiology, Showa University School of Dentistry, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.
Daisuke YoshimaruDivision of Regenerative Medicine, The Jikei University School of Medicine, 3-25-8 Nishi-Shimbashi, Minato-ku, Tokyo 105-8461, Japan; RIKEN Center for Brain Science, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan.
Junichi HataDivision of Regenerative Medicine, The Jikei University School of Medicine, 3-25-8 Nishi-Shimbashi, Minato-ku, Tokyo 105-8461, Japan; RIKEN Center for Brain Science, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan; Graduate School of Human Health Sciences, Tokyo Metropolitan University, 7-2-10 Higashiogu, Arakawa-ku, Tokyo 116-8551, Japan.
Mami MatsumotoSection of Electron Microscopy, Supportive Center for Brain Research, National Institute for Physiological Sciences, Okazaki, Aichi 444-8585, Japan; Department of Developmental and Regenerative Neurobiology, Institute of Brain Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi 467-8601, Japan.
Shu TairaFaculty of Food and Agricultural Sciences, Fukushima University, Kanayagawa, Fukushima 960-1248, Japan.
Hiroyoshi TakeuchiDepartment of Psychiatry, Keio University School of Medicine, Tokyo 160-8582, Japan.
Hideyuki OkanoRIKEN Center for Brain Science, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan; Department of Physiology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Nobuhiko OhnoDivision of Histology and Cell Biology, Department of Anatomy, Jichi Medical University School of Medicine, Shimotsuke, Tochigi 329-0498, Japan; Division of Ultrastructural Research, National Institute for Physiological Sciences, Okazaki 444-8787, Japan.
Makoto SuematsuDepartment of Biochemistry, Keio University School of Medicine, Tokyo 160-8582, Japan.
Tomio InoueDepartment of Oral Physiology, Showa University School of Dentistry, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.
Atsushi NambuDivision of System Neurophysiology, National Institute for Physiological Sciences, 38 Nishigonaka, Myodaiji, Okazaki, Aichi 444-8585, Japan; Department of Physiological Sciences, SOKENDAI (The Graduate University for Advanced Studies), 38 Nishigonaka, Myodaiji, Okazaki, Aichi 444-8585, Japan.
Masahiko WatanabeDepartment of Anatomy and Embryology, University of Hokkaido, Sapporo, Hokkaido 060-8638, Japan.
Kenji F TanakaDivision of Brain Sciences, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo 160-8582, Japan. Electronic address: kftanaka@keio.jp.
Keio University · JPShowa University · JPJikei University School of Medicine · JPThe Graduate University for Advanced Studies, SOKENDAI · JPFukushima University · JPHokkaido University · JPJichi Medical University · JPNagoya City University · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dyskinesia is involuntary movement caused by long-term medication with dopamine-related agents: the dopamine agonist 3,4-dihydroxy-L-phenylalanine (L-DOPA) to treat Parkinson's disease (L-DOPA-induced dyskinesia [LID]) or dopamine antagonists to treat schizophrenia (tardive dyskinesia [TD]). However, it remains unknown why distinct types of medications for distinct neuropsychiatric disorders induce similar involuntary movements. Here, we search for a shared structural footprint using magnetic resonance imaging-based macroscopic screening and super-resolution microscopy-based microscopic identification. We identify the enlarged axon terminals of striatal medium spiny neurons in LID and TD model mice. Striatal overexpression of the vesicular gamma-aminobutyric acid transporter (VGAT) is necessary and sufficient for modeling these structural changes; VGAT levels gate the functional and behavioral alterations in dyskinesia models. Our findings indicate that lowered type 2 dopamine receptor signaling with repetitive dopamine fluctuations is a common cause of VGAT overexpression and late-onset dyskinesia formation and that reducing dopamine fluctuation rescues dyskinesia pathology via VGAT downregulation.

Indexed as

Dyskinesia, Drug-InducedParkinsonian DisordersAnimalsAntiparkinson AgentsDopamineDopamine Agonistsgamma-Aminobutyric AcidLevodopaMiceOxidopamineAntiparkinson AgentsDopamineDopamine Agonistsgamma-Aminobutyric AcidLevodopaOxidopaminebrain volumedopamine fluctuationGABAGPeL-DOPA-induced dyskinesiamedium spiny neuronSNrstructural plasticitytardive dyskinesiaVGAT

Identifiers

PMID37774703
PMCPMC10591040
OpenAlexW4387131736

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.