Evidence map›Paper›PMID 21821100›Full record

ArticleNeuroscience2011

Relationship between noise-induced hearing-loss, persistent tinnitus and growth-associated protein-43 expression in the rat cochlear nucleus: does synaptic plasticity in ventral cochlear nucleus suppress tinnitus?

K S Kraus, D Ding, H Jiang, E Lobarinas, W Sun, R J Salvi

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.7field-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

44 citing papers in PubMed, 62 citations in OpenAlex.

  1. NMDA Receptors: Next therapeutic targets for Tinnitus?Biochemistry and biophysics reports · 2025
    Review
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  16. Effects of Acoustic Environment on Tinnitus Behavior in Sound-Exposed Rats.Journal of the Association for Research in Otolaryngology : JARO · 2018
    Article
  17. Article
  18. Article
  19. Article
  20. Noise-induced hearing loss: Neuropathic pain via Ntrk1 signaling.Molecular and cellular neurosciences · 2016
    Article
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

6 authors at 1 institution in 1 country.

K S KrausCenter for Hearing and Deafness, State University of New York at Buffalo, 137 Cary Hall, 3435 Main Street, Buffalo, NY 14214, USA. kraus.ks@gmail.com
D Ding
H Jiang
E Lobarinas
W Sun
R J Salvi
University at Buffalo, State University of New York · US

Funding

Animal Models of Tinnitus, Brain Imaging & TherapyR01DC009091 · NIDCD · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI SALVI, RICHARD J · 2007 to 2011
$2.9M
Neural Aspects of TinnitusR01DC009219 · NIDCD · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI SALVI, RICHARD J · 2008 to 2012
$1.6M
NIDCD NIH HHS R01 DC009091NIDCD NIH HHS R01 DC009219NIDCD NIH HHS R01DC009219
6 · The paper itself

Abstract

Aberrant, lesion-induced neuroplastic changes in the auditory pathway are believed to give rise to the phantom sound of tinnitus. Noise-induced cochlear damage can induce extensive fiber growth and synaptogenesis in the cochlear nucleus, but it is currently unclear if these changes are linked to tinnitus. To address this issue, we unilaterally exposed nine rats to narrow-band noise centered at 12 kHz at 126 dB sound pressure level (SPL) for 2 h and sacrificed them 10 weeks later for evaluation of synaptic plasticity (growth-associated protein 43 [GAP-43] expression) in the cochlear nucleus. Noise-exposed rats along with three age-matched controls were screened for tinnitus-like behavior with gap prepulse inhibition of the acoustic startle (GPIAS) before, 1-10 days after, and 8-10 weeks after the noise exposure. All nine noise-exposed rats showed similar patterns of severe hair cell loss at high- and mid-frequency regions in the exposed ear. Eight of the nine showed strong up-regulation of GAP-43 in auditory nerve fibers and pronounced shrinkage of the ventral cochlear nucleus (VCN) on the noise-exposed side, and strong up-regulation of GAP-43 in the medial ventral VCN, but not in the lateral VCN or the dorsal cochlear nucleus. GAP-43 up-regulation in VCN was significantly greater in Noise-No-Tinnitus rats than in Noise-Tinnitus rats. One Noise-No-Tinnitus rat showed no up-regulation of GAP-43 in auditory nerve fibers and only little VCN shrinkage, suggesting that auditory nerve degeneration plays a role in tinnitus generation. Our results suggest that noise-induced tinnitus is suppressed by strong up-regulation of GAP-43 in the medial VCN. GAP-43 up-regulation most likely originates from medial olivocochlear neurons. Their increased excitatory input on inhibitory neurons in VCN may possibly reduce central hyperactivity and tinnitus.

Indexed as

AnimalsCochlear NucleusDisease Models, AnimalGAP-43 ProteinHearing Loss, Noise-InducedMaleNeuronal PlasticityRatsRats, Sprague-DawleySynapsesTinnitusUp-RegulationGAP-43 Protein

Identifiers

PMID21821100
PMCPMC3390756
OpenAlexW233156525

What OpenQuestion holds

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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.