Evidence map›Paper›PMID 28011083›Full record

ArticleHearing research2017

Impaired auditory processing and altered structure of the endbulb of Held synapse in mice lacking the GluA3 subunit of AMPA receptors.

Sofía García-Hernández, Manabu Abe, Kenji Sakimura, María E Rubio

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Hearing research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.4field-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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Altered Auditory Maturation in Fragile X Syndrome and Its Involvement in Audiogenic Seizure Susceptibility.Autism research : official journal of the International Society for Autism Research · 2026
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  12. Mechanisms and Functional Consequences of Presynaptic Homeostatic Plasticity at Auditory Nerve Synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
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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

4 authors at 3 institutions in 2 countries.

Sofía García-HernándezDepartment of Otolaryngology, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.
Manabu AbeNiigata University Brain Research Institute, Japan.
Kenji SakimuraNiigata University Brain Research Institute, Japan.
María E RubioDepartment of Otolaryngology, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA; Department of Neurobiology, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA; Center for the Neural Basis of Cognition, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA. Electronic address: mer@pitt.edu.
Niigata University · JPCenter for the Neural Basis of Cognition · USUniversity of Pittsburgh · US

Funding

Mechanisms of hypersensitivity to sound-induced cochlear damageR01DC013048 · NIDCD · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Maria-Eulalia Rubio-Valero · 2013 to 2026
$6.8M
NIDCD NIH HHS R01 DC013048
6 · The paper itself

Abstract

AMPA glutamate receptor complexes with fast kinetics conferred by subunits like GluA3 and GluA4 are essential for temporal precision of synaptic transmission. The specific role of GluA3 in auditory processing and experience related changes in the auditory brainstem remain unknown. We investigated the role of the GluA3 in auditory processing by using wild type (WT) and GluA3 knockout (GluA3-KO) mice. We recorded auditory brainstem responses (ABR) to assess auditory function and used electron microscopy to evaluate the ultrastructure of the auditory nerve synapse on bushy cells (AN-BC synapse). Since labeling for GluA3 subunit increases on auditory nerve synapses within the cochlear nucleus in response to transient sound reduction, we investigated the role of GluA3 in experience-dependent changes in auditory processing. We induced transient sound reduction by plugging one ear and evaluated ABR threshold and peak amplitude recovery for up to 60 days after ear plug removal in WT and GluA3-KO mice. We found that the deletion of GluA3 leads to impaired auditory signaling that is reflected in decreased ABR peak amplitudes, an increased latency of peak 2, early onset hearing loss and reduced numbers and sizes of postsynaptic densities (PSDs) of AN-BC synapses. Additionally, the lack of GluA3 hampers ABR threshold recovery after transient ear plugging. We conclude that GluA3 is required for normal auditory signaling, normal ultrastructure of AN-BC synapses in the cochlear nucleus and normal experience-dependent changes in auditory processing after transient sound reduction.

Indexed as

Auditory PerceptionBehavior, AnimalHearingAcoustic StimulationAdaptation, PhysiologicalAnimalsCochlear NerveCochlear NucleusEvoked Potentials, Auditory, Brain StemGenetic Predisposition to DiseaseHearing Loss, High-FrequencyMaleMice, Inbred C57BLMice, KnockoutPhenotypeReaction Timeglutamate receptor ionotropic, AMPA 3Receptors, AMPAAuditory brainstemAuditory experienceCochlear nucleusEndbulb of Held synapsesPostsynaptic densityUltrastructure

Identifiers

PMID28011083
PMCPMC5240188
OpenAlexW2562174218

What OpenQuestion holds

Textmetadata
LicenceTDM
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.