Evidence map›Paper›PMID 42737467›Full record

ArticleInternational journal of molecular sciences2026

Altered Excitation-Inhibition Balance and mGluR

Hongseong Shin, Yoon Ji Kwon, Hyunjung Hwang, Taewoo Ko, Eun Bi Choi, Yang Tae Kim, Yu Mi Han, Jae Geun Kim, Qiang Zhou, Sungchil Yang and 1 more

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Article in International journal of molecular sciences, 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
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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

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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

11 authors.

Hongseong ShinDepartment of Nanobioengineering, Incheon National University, Incheon 22012, Republic of Korea.ORCID 0009-0001-4335-3354
Yoon Ji KwonDepartment of Neuroscience, City University of Hong Kong, 83 Tat Chee Avenue, Kowloon, Hong Kong SAR, China.ORCID 0000-0001-6676-0131
Hyunjung HwangDepartment of Nanobioengineering, Incheon National University, Incheon 22012, Republic of Korea.ORCID 0009-0001-9932-6152
Taewoo KoDepartment of Nanobioengineering, Incheon National University, Incheon 22012, Republic of Korea.
Eun Bi ChoiDivision of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, Republic of Korea.
Yang Tae KimDivision of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, Republic of Korea.
Yu Mi HanResearch Institute of Medical Science, Sungkyunkwan University School of Medicine, Seoul 16419, Republic of Korea.
Jae Geun KimCenter for Brain-Machine Interface, Incheon National University, Incheon 22012, Republic of Korea.
Qiang ZhouState Key Laboratory of Chemical Oncogenomics, Guangdong Provincial Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen 518055, China.ORCID 0000-0001-7172-2500
Sungchil YangDepartment of Neuroscience, City University of Hong Kong, 83 Tat Chee Avenue, Kowloon, Hong Kong SAR, China.
Sunggu YangDepartment of Nanobioengineering, Incheon National University, Incheon 22012, Republic of Korea.

Funding

National Research Foundation of Korea RS-2022-NR069408
6 · The paper itself

Abstract

Parkinson's disease (PD) is characterized by progressive dopaminergic degeneration and maladaptive motor cortical plasticity. However, the cellular pathways underlying cortical surface activity in the primary motor cortex (M1) remain unclear, despite serving as a potential target for electrotherapy. We investigated the excitatory-inhibitory (E-I) balance and synaptic plasticity of superficial M1 circuits in a unilateral 6-hydroxydopamine (6-OHDA)-induced rat model of PD. Using extracellular local field potential and whole-cell patch recordings from the contralateral and ipsilateral M1 hemispheres of hemi-parkinsonian rats, we observed a significantly elevated field excitatory postsynaptic potential (fEPSP) input-output function but unchanged intrinsic neuronal excitability in the M1 superficial layer. An altered relative contribution between alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)- and N-methyl-D-aspartate receptor (NMDAR)-mediated transmission was reflected by a significantly increased AMPA/NMDA ratio. Markedly reduced inhibitory synaptic tone was also evidenced by the decreased amplitude and frequency of spontaneous inhibitory postsynaptic currents (sIPSCs), supporting an E-I imbalance favoring excitation in PD. Furthermore, group I metabotropic glutamate receptor (mGluR

Indexed as

Motor CortexNeuronal PlasticityParkinson DiseaseReceptor, Metabotropic Glutamate 5Receptors, Metabotropic GlutamateAnimalsDisease Models, AnimalExcitatory Postsynaptic PotentialsMaleOxidopamineRatsRats, Sprague-DawleyReceptors, AMPAGrm5 protein, ratmetabotropic glutamate receptor type 1OxidopamineReceptor, Metabotropic Glutamate 5Receptors, AMPAReceptors, Metabotropic Glutamatemetabotropic glutamate receptormotor cortexParkinson’s diseasesensorimotor deficitssynaptic plasticity

Identifiers

PMID42737467
PMCPMC13565811

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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.