Evidence map›Paper›PMID 30123822›Full record

ArticleeNeuro

Central Compensation in Auditory Brainstem after Damaging Noise Exposure.

Katrina M Schrode, Michael A Muniak, Ye-Hyun Kim, Amanda M Lauer

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

51 citing papers in PubMed, 70 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Katrina M SchrodeDepartment of Otolaryngology, Johns Hopkins School of Medicine, Baltimore, MD 21205.ORCID 0000-0002-9963-9642
Michael A MuniakHearing Research, Garvan Institute of Medical Research, Sydney, NSW 2010, Australia.ORCID 0000-0001-8047-5871
Ye-Hyun KimDepartment of Otolaryngology, Johns Hopkins School of Medicine, Baltimore, MD 21205.
Amanda M LauerDepartment of Otolaryngology, Johns Hopkins School of Medicine, Baltimore, MD 21205.
Johns Hopkins University · USGarvan Institute of Medical Research · AU

Funding

Training Program in Hearing and BalanceT32DC000023 · NIDCD · JOHNS HOPKINS UNIVERSITY · PI CULLEN, KATHLEEN E · 1989 to 2025
$8.7M
Supplement for temporal bone tissue scanning equipmentR01DC016641 · NIDCD · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI DENT, MICHEAL L, LAUER, AMANDA M. · 2018 to 2022
$2.2M
Perceptual and central auditory consequences of noise-induced hearing lossR03DC012352 · NIDCD · JOHNS HOPKINS UNIVERSITY · PI LAUER, AMANDA M. · 2013 to 2015
$495k
NIDCD NIH HHS R01 DC016641NIDCD NIH HHS R03 DC012352NIDCD NIH HHS T32 DC000023
6 · The paper itself

Abstract

Noise exposure is one of the most common causes of hearing loss and peripheral damage to the auditory system. A growing literature suggests that the auditory system can compensate for peripheral loss through increased central neural activity. The current study sought to investigate the link between noise exposure, increases in central gain, synaptic reorganization, and auditory function. All axons of the auditory nerve project to the cochlear nucleus, making it a requisite nucleus for sound detection. As the first synapse in the central auditory system, the cochlear nucleus is well positioned to respond plastically to loss of peripheral input. To investigate noise-induced compensation in the central auditory system, we measured auditory brainstem responses (ABRs) and auditory perception and collected tissue from mice exposed to broadband noise. Noise-exposed mice showed elevated ABR thresholds, reduced ABR wave 1 amplitudes, and spiral ganglion neuron loss. Despite peripheral damage, noise-exposed mice were hyperreactive to loud sounds and showed nearly normal behavioral sound detection thresholds. Ratios of late ABR peaks (2-4) relative to the first ABR peak indicated that brainstem pathways were hyperactive in noise-exposed mice, while anatomical analysis indicated there was an imbalance between expression of excitatory and inhibitory proteins in the ventral cochlear nucleus. The results of the current study suggest that a reorganization of excitation and inhibition in the ventral cochlear nucleus may drive hyperactivity in the central auditory system. This increase in central gain can compensate for peripheral loss to restore some aspects of auditory function.

Indexed as

AnimalsAuditory PerceptionAuditory ThresholdBehavior, AnimalCochlear NucleusEvoked Potentials, Auditory, Brain StemFemaleHyperkinesisMaleMiceMice, Inbred CBANoiseSpiral GanglionAuditorybrainstemcompensationhyperactivity

Identifiers

PMID30123822
PMCPMC6096756
OpenAlexW2884989748

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.