Evidence map›Paper›PMID 34431014›Full record

ArticleNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2021

"Glu/GABA-Gln" metabolic loop abnormalities in iminodipropionitrile (IDPN)-induced dyskinetic syndrome.

Juanjuan Hao, Keyu Jiang, Xin Zhang, Min Wu, Bitao Ma

Abstract read
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In one paragraph

Article in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 36% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
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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

5 authors at 1 institution in 1 country.

Juanjuan Hao *School of Medicine, Shaoxing University, 900 Chengnan Road, Shaoxing, 312000, People's Republic of China.
Keyu Jiang *Xin Hua Hospital Affiliated To Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Shanghai, 200092, People's Republic of China.
Xin ZhangXin Hua Hospital Affiliated To Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Shanghai, 200092, People's Republic of China.
Min WuXin Hua Hospital Affiliated To Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Shanghai, 200092, People's Republic of China. wumin@xinhuamed.com.cn.
Bitao MaXin Hua Hospital Affiliated To Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Shanghai, 200092, People's Republic of China. wumin@xinhuamed.com.cn.ORCID http://orcid.org/0000-0002-5101-9356
Shanghai Jiao Tong University · CN

Funding

Shanghai Jiaotong University School of Medicine high level local college construction project No 18zxy006Shanghai Municipal Health Commission No 2018LQ010Shanghai Science and Technology Commission Research Project No 18401902700;No 17401931200Shaoxing University college-level research projects No 20205038;No 2020LG1007the national natural science foundation of china No 81874486;the national natural science foundation of china No 82004418
6 · The paper itself

Abstract

objectiveIminodipropionitrile (IDPN)-induced dyskinetic syndrome is characterized by abnormal repetitive involuntary movements with abnormalities in the neuro-transmission. This study explored the mechanism of glutamate (Glu)/γ-aminobutyric acid (GABA)-glutamine (Gln) metabolic circuit in rat dyskinetic syndrome and the possible regulation mechanism of "tiapride (Tia)."

methodsMale Wistar rats were assigned to the control group, dyskinetic syndrome group, and Tia group. Dyskinetic syndrome was induced by injecting with 3,3'-iminodipropionitrile for 7 days. Tia group was treated with tiapride, while the control and dyskinetic syndrome groups were gavaged with saline. Eventually the Glu, GABA, and Gln concentrations in striatum were detected using UPLC-3QMS, additionally another amino acid neurotransmitters (aspartate, glycine) were also detected. Expressions of glutamine synthetase (GS), glutamate transporter (EAAT

resultsThe behavior test scores of dyskinetic syndrome group were increased compared with the control group. Tia group decreased the behavior test scores compared with dyskinetic syndrome group. For amino acid neuro-transmission, dyskinetic syndrome group increased Glu level (p < 0.01), decreased GABA level (p < 0.01), increased Glu/GABA ratio (p < 0.01), and decreased Asp level (p < 0.01) compared with control group. Tia group decreased Glu level (p < 0.01), increased GABA level (p < 0.01), decreased Glu/GABA ratio (p < 0.01), and increased Asp level (p < 0.05) compared with dyskinetic syndrome group. For Glu/GABA-Gln circuit, the protein and mRNA expression of GS and EAAT

conclusionThe rat dyskinetic syndrome has Glu/GABA-Gln abnormalities. "Tiapride" upregulated the protein expression of GS and EAAT

Indexed as

DyskinesiasGlutamic AcidAnimalsgamma-Aminobutyric AcidGlutamineMaleRatsRats, Wistargamma-Aminobutyric AcidGlutamic AcidGlutamineAmino acid neurotransmittersGlutamic acid/γ-aminobutyric acid–glutamine metabolism loopThe rat dyskinetic syndromeTiapride

Identifiers

PMID34431014
OpenAlexW3194383096

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.