Evidence map›Paper›PMID 27924869›Full record

ArticleNature communications2016

ASIC1a regulates insular long-term depression and is required for the extinction of conditioned taste aversion.

Wei-Guang Li, Ming-Gang Liu, Shining Deng, Yan-Mei Liu, Lin Shang, Jing Ding, Tsan-Ting Hsu, Qin Jiang, Ying Li, Fei Li and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

36 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
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  8. Possible Compensatory Role of ASICs in Glutamatergic Synapses.International journal of molecular sciences · 2023
    Article
  9. Review
  10. Intoxicating effects of alcohol depend on acid-sensing ion channels.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Article
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  15. Acid-Sensing Ion Channels and Mechanosensation.International journal of molecular sciences · 2021
    Review
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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

12 authors at 4 institutions in 3 countries.

Wei-Guang LiDiscipline of Neuroscience, Department of Anatomy, Histology and Embryology, and Collaborative Innovation Center for Brain Science, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Ming-Gang LiuDiscipline of Neuroscience, Department of Anatomy, Histology and Embryology, and Collaborative Innovation Center for Brain Science, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Shining DengDepartment of Developmental and Behavioral Pediatrics, Shanghai Institute of Pediatric Translational Medicine, Shanghai Children's Medical Center, Ministry of Education-Shanghai Key Laboratory of Children's Environmental Health, Shanghai Jiao Tong University School of Medicine, Shanghai 200129, China.
Yan-Mei LiuDiscipline of Neuroscience, Department of Anatomy, Histology and Embryology, and Collaborative Innovation Center for Brain Science, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Lin ShangDepartment of Developmental and Behavioral Pediatrics, Shanghai Institute of Pediatric Translational Medicine, Shanghai Children's Medical Center, Ministry of Education-Shanghai Key Laboratory of Children's Environmental Health, Shanghai Jiao Tong University School of Medicine, Shanghai 200129, China.
Jing DingDepartment of Developmental and Behavioral Pediatrics, Shanghai Institute of Pediatric Translational Medicine, Shanghai Children's Medical Center, Ministry of Education-Shanghai Key Laboratory of Children's Environmental Health, Shanghai Jiao Tong University School of Medicine, Shanghai 200129, China.
Tsan-Ting HsuInstitute of Neuroscience, National Yang-Ming University, 155, Section 2, Li-Nong Street, Taipei 112, Taiwan.
Qin JiangDiscipline of Neuroscience, Department of Anatomy, Histology and Embryology, and Collaborative Innovation Center for Brain Science, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Ying LiDiscipline of Neuroscience, Department of Anatomy, Histology and Embryology, and Collaborative Innovation Center for Brain Science, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Fei LiDepartment of Developmental and Behavioral Pediatrics, Shanghai Institute of Pediatric Translational Medicine, Shanghai Children's Medical Center, Ministry of Education-Shanghai Key Laboratory of Children's Environmental Health, Shanghai Jiao Tong University School of Medicine, Shanghai 200129, China.
Michael Xi ZhuDepartment of Integrative Biology and Pharmacology, The University of Texas Health Science Center at Houston, Houston, Texas 77030, USA.
Tian-Le XuDiscipline of Neuroscience, Department of Anatomy, Histology and Embryology, and Collaborative Innovation Center for Brain Science, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Shanghai Jiao Tong University · CNShanghai Children's Medical Center · CNNational Yang Ming Chiao Tung University · TWThe University of Texas Health Science Center at Houston · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acid-sensing ion channel 1a (ASIC1a) has been shown to play important roles in synaptic plasticity, learning and memory. Here we identify a crucial role for ASIC1a in long-term depression (LTD) at mouse insular synapses. Genetic ablation and pharmacological inhibition of ASIC1a reduced the induction probability of LTD without affecting that of long-term potentiation in the insular cortex. The disruption of ASIC1a also attenuated the extinction of established taste aversion memory without altering the initial associative taste learning or its long-term retention. Extinction of taste aversive memory led to the reduced insular synaptic efficacy, which precluded further LTD induction. The impaired LTD and extinction learning in ASIC1a null mice were restored by virus-mediated expression of wild-type ASIC1a, but not its ion-impermeable mutant, in the insular cortices. Our data demonstrate the involvement of an ASIC1a-mediated insular synaptic depression mechanism in extinction learning, which raises the possibility of targeting ASIC1a to manage adaptive behaviours.

Indexed as

Conditioning, ClassicalExtinction, PsychologicalLong-Term PotentiationAcid Sensing Ion ChannelsAmino Acid SequenceAnimalsAvoidance LearningCerebral CortexElectric StimulationGlutamatesGlycineGlycogen Synthase Kinase 3 betaMaleMemoryMice, Inbred C57BLPeptides3,5-dihydroxyphenylglycineAcid Sensing Ion ChannelsASIC1 protein, mouseGlutamatesGlycineGlycogen Synthase Kinase 3 betaPeptidesResorcinols

Identifiers

PMID27924869
PMCPMC5150990
OpenAlexW2559976454

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.