Evidence map›Paper›PMID 37351424›Full record

ArticleFrontiers in neuroscience2023

Axon terminal hypertrophy of striatal projection neurons with levodopa-induced dyskinesia priming.

Takashi Nakamura, Haruo Nishijima, Fumiaki Mori, Iku Kinoshita, Tomoya Kon, Chieko Suzuki, Koichi Wakabayashi, Masahiko Tomiyama

Abstract read
In one paragraph

Article in Frontiers in neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

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

8 authors.

Takashi NakamuraDepartment of Neurology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Haruo NishijimaDepartment of Neurology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Fumiaki MoriDepartment of Neuropathology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Iku KinoshitaDepartment of Neurology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Tomoya KonDepartment of Neurology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Chieko SuzukiDepartment of Neurology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Koichi WakabayashiDepartment of Neuropathology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Masahiko TomiyamaDepartment of Neurology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: A rat model of levodopa-induced dyskinesia (LID) showed enlarged axon terminals of striatal direct pathway neurons in the internal segment of the globus pallidus (GPi) with excessive gamma-aminobutyric acid (GABA) storage in them. Massive GABA release to GPi upon levodopa administration determines the emergence of LID. Objectives: We examined whether LID and axon terminal hypertrophy gradually develop with repeated levodopa treatment in Parkinsonian rats to examine if the hypertrophy reflects dyskinesia priming. Methods: 6-hydroxydopamine-lesioned hemiparkinsonian rats were randomly allocated to receive saline injections (placebo group, 14 days; Results: The AIM score increased with levodopa treatment, as did the hypertrophy of axon terminals in the GPi, showing an increased number of synaptic vesicles in hypertrophied terminals. Conclusion: Increased GABA storage in axon terminals of the direct pathway neurons represents the priming process of LID.

Indexed as

abnormal involuntary movementaxon terminalsGABAlevodopa-treated ratsprimingsynaptic plasticitysynaptic vesicles

Identifiers

PMID37351424
PMCPMC10282195

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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.