Evidence map›Paper›PMID 39196683›Full record

ArticleNeuropsychopharmacology reports2024

Proline-rich transmembrane protein 2 regulates the magnitude and frequency of dopamine release by repetitive neuronal stimuli in the striatum of L-dopa-treated mice.

Daisuke Hatta, Shiho Makiya, Kaito Kanamoto, Kaori Watanabe, Yuki Fuchigami, Shigeru Kawakami, Akira Kinoshita, Koh-Ichiro Yoshiura, Naohiro Kurotaki, Keiro Shirotani and 1 more

Abstract read
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In one paragraph

Article in Neuropsychopharmacology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

11 authors.

Daisuke HattaDepartment of Genome-Based Drug Discovery, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.ORCID 0000-0001-7972-1852
Shiho MakiyaDepartment of Genome-Based Drug Discovery, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.
Kaito KanamotoDepartment of Genome-Based Drug Discovery, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.
Kaori WatanabeDepartment of Genome-Based Drug Discovery, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.
Yuki FuchigamiDepartment of Pharmaceutical Informatics, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.
Shigeru KawakamiDepartment of Pharmaceutical Informatics, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.
Akira KinoshitaDepartment of Human Genetics, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.
Koh-Ichiro YoshiuraDepartment of Human Genetics, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.
Naohiro KurotakiDepartment of Human Genetics, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.
Keiro ShirotaniDepartment of Genome-Based Drug Discovery, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.
Nobuhisa IwataDepartment of Genome-Based Drug Discovery, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.ORCID 0000-0001-8721-7947

Funding

Japan Agency for Medical Research and Development JP16ek0109119hJapan Society for the Promotion of Science 18H02720Japan Society for the Promotion of Science 20K22688Japan Society for the Promotion of Science 21H02809
6 · The paper itself

Abstract

Mutations in proline-rich transmembrane protein 2 (PRRT2) cause paroxysmal kinesigenic dyskinesia (PKD). Recently, we reported that a Prrt2 mutation exacerbated L-dopa-induced motor deficits in mice, suggesting that the basal ganglia might contribute to PKD pathology. Here, we demonstrated that the Prrt2 mutation enhanced depolarization stimuli-induced extracellular dopamine levels in the mouse striatum, which were attenuated by repeated stimulation. L-dopa administration maintained high dopamine levels in Prrt2-KI mice even during repetitive stimuli but did not affect dopamine levels in wild-type mice. Thus, the enhanced and prolonged responsiveness of dopamine release in nigrostriatal dopaminergic neurons to sequential excitation may be partially implicated in Prrt2-related dyskinesia.

Indexed as

Corpus StriatumDopamineLevodopaMembrane ProteinsNerve Tissue ProteinsAnimalsDopamine AgentsMaleMiceMice, Inbred C57BLMice, TransgenicMutationDopamineDopamine AgentsLevodopaMembrane ProteinsNerve Tissue ProteinsPRRT2 protein, mousedopamineL‐dopaPrrt2

Identifiers

PMID39196683
PMCPMC11609736

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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.