Evidence map›Paper›PMID 31101759›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019

Protein Kinase C Lambda Mediates Acid-Sensing Ion Channel 1a-Dependent Cortical Synaptic Plasticity and Pain Hypersensitivity.

Hu-Song Li, Xin-Yu Su, Xing-Lei Song, Xin Qi, Ying Li, Rui-Qi Wang, Oleksandr Maximyuk, Oleg Krishtal, Tingting Wang, Houqin Fang and 6 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Acid-sensing ion channels as sensors of brain metabolic state.Pflugers Archiv : European journal of physiology · 2026
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  8. Possible Compensatory Role of ASICs in Glutamatergic Synapses.International journal of molecular sciences · 2023
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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

16 authors at 5 institutions in 3 countries.

Hu-Song LiCollaborative Innovation Center for Brain Science, Department of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.ORCID 0000-0003-1186-1917
Xin-Yu SuCollaborative Innovation Center for Brain Science, Department of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Xing-Lei SongCollaborative Innovation Center for Brain Science, Department of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Xin QiCollaborative Innovation Center for Brain Science, Department of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Ying LiCollaborative Innovation Center for Brain Science, Department of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Rui-Qi WangCollaborative Innovation Center for Brain Science, Department of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.ORCID 0000-0001-7176-9560
Oleksandr MaximyukBogomoletz Institute of Physiology of NAS Ukraine, 01024 Kyiv, Ukraine.ORCID 0000-0003-3288-4974
Oleg KrishtalBogomoletz Institute of Physiology of NAS Ukraine, 01024 Kyiv, Ukraine.ORCID 0000-0003-3342-9930
Tingting WangShanghai Key Laboratory of Regulatory Biology, and Shanghai Key Laboratory of Brain Functional Genomics, School of Life Sciences, East China Normal University, Shanghai 200241, China.
Houqin FangShanghai Key Laboratory of Regulatory Biology, and Shanghai Key Laboratory of Brain Functional Genomics, School of Life Sciences, East China Normal University, Shanghai 200241, China.
Lujian LiaoShanghai Key Laboratory of Regulatory Biology, and Shanghai Key Laboratory of Brain Functional Genomics, School of Life Sciences, East China Normal University, Shanghai 200241, China.
Hong CaoState Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institute of Brain Science, Fudan University, Shanghai 200032, China, and.ORCID 0000-0001-5048-3379
Yu-Qiu ZhangState Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institute of Brain Science, Fudan University, Shanghai 200032, China, and.ORCID 0000-0001-6623-9629
Michael X ZhuDepartment of Integrative Biology and Pharmacology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, Texas 77030.ORCID 0000-0002-5676-841X
Ming-Gang LiuCollaborative Innovation Center for Brain Science, Department of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China, lmg11302000@126.com xu-happiness@shsmu.edu.cn.
Tian-Le XuCollaborative Innovation Center for Brain Science, Department of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China, lmg11302000@126.com xu-happiness@shsmu.edu.cn.
Shanghai Jiao Tong University · CNEast China Normal University · CNBogomoletz Institute of Physiology · UAFudan University · CNThe University of Texas Health Science Center at Houston · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic pain is a serious debilitating disease for which effective treatment is still lacking. Acid-sensing ion channel 1a (ASIC1a) has been implicated in nociceptive processing at both peripheral and spinal neurons. However, whether ASIC1a also contributes to pain perception at the supraspinal level remains elusive. Here, we report that ASIC1a in ACC is required for thermal and mechanical hypersensitivity associated with chronic pain. ACC-specific genetic deletion or pharmacological blockade of ASIC1a reduced the probability of cortical LTP induction and attenuated inflammatory thermal hyperalgesia and mechanical allodynia in male mice. Using cell type-specific manipulations, we demonstrate that ASIC1a in excitatory neurons of ACC is a major player in cortical LTP and pain behavior. Mechanistically, we show that ASIC1a tuned pain-related cortical plasticity through protein kinase C λ-mediated increase of membrane trafficking of AMPAR subunit GluA1 in ACC. Importantly, postapplication of ASIC1a inhibitors in ACC reversed previously established nociceptive hypersensitivity in both chronic inflammatory pain and neuropathic pain models. These results suggest that ASIC1a critically contributes to a higher level of pain processing through synaptic potentiation in ACC, which may serve as a promising analgesic target for treatment of chronic pain.

Indexed as

6-Cyano-7-nitroquinoxaline-2,3-dioneAcid Sensing Ion ChannelsAnimalsCells, CulturedGyrus CinguliIsoenzymesMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMicroinjectionsNeuralgiaNeuronal PlasticityOrgan Culture TechniquesPain Measurement6-Cyano-7-nitroquinoxaline-2,3-dioneAcid Sensing Ion ChannelsASIC1 protein, mouseIsoenzymesProtein Kinase CProtein Kinase C-lambdaACCacid-sensing ion channelchronic painlong-term potentiationprotein kinase C

Identifiers

PMID31101759
PMCPMC6636072
OpenAlexW2946395141

What OpenQuestion holds

Textmetadata
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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.