Evidence map›Paper›PMID 26312501›Full record

ArticleeLife2015

Noise-induced plasticity of KCNQ2/3 and HCN channels underlies vulnerability and resilience to tinnitus.

Shuang Li, Bopanna I Kalappa, Thanos Tzounopoulos

Abstract read
In one paragraph

Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
–field-weighted citation impact
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

43 citing papers in PubMed.

  1. Article
  2. A discrete serotonergic circuit involved in the generation of tinnitus behavior.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Neuroscientific therapies for subjective tinnitus.Journal of Zhejiang University. Science. B · 2026
    Review
  4. Article
  5. Inhibition of Cortical Evoked Responses to Sound Pulses by Preceding Silent Gaps.Journal of the Association for Research in Otolaryngology : JARO · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. A Role for KCNQ Channels on Cell Type-Specific Plasticity in Mouse Auditory Cortex after Peripheral Damage.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Sparsely Distributed, Pre-synaptic Kv3 KFrontiers in cellular neuroscience · 2021
    Article
  18. Article
  19. Article
  20. 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

3 authors.

Shuang LiDepartments of Otolaryngology and Neurobiology, University of Pittsburgh School of Medicine, Pittsburgh, United States.
Bopanna I KalappaDepartments of Otolaryngology and Neurobiology, University of Pittsburgh School of Medicine, Pittsburgh, United States.
Thanos TzounopoulosDepartments of Otolaryngology and Neurobiology, University of Pittsburgh School of Medicine, Pittsburgh, United States.

Funding

Cell-specific Synaptic Plasticity in the Auditory BrainstemR01DC007905 · NIDCD · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI TZOUNOPOULOS, THANOS · 2007 to 2021
$6.9M
NIDCD NIH HHS DC-DC007905NIDCD NIH HHS R01 DC007905
6 · The paper itself

Abstract

Vulnerability to noise-induced tinnitus is associated with increased spontaneous firing rate in dorsal cochlear nucleus principal neurons, fusiform cells. This hyperactivity is caused, at least in part, by decreased Kv7.2/3 (KCNQ2/3) potassium currents. However, the biophysical mechanisms underlying resilience to tinnitus, which is observed in noise-exposed mice that do not develop tinnitus (non-tinnitus mice), remain unknown. Our results show that noise exposure induces, on average, a reduction in KCNQ2/3 channel activity in fusiform cells in noise-exposed mice by 4 days after exposure. Tinnitus is developed in mice that do not compensate for this reduction within the next 3 days. Resilience to tinnitus is developed in mice that show a re-emergence of KCNQ2/3 channel activity and a reduction in HCN channel activity. Our results highlight KCNQ2/3 and HCN channels as potential targets for designing novel therapeutics that may promote resilience to tinnitus.

Indexed as

NoiseAnimalsHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsKCNQ2 Potassium ChannelKCNQ3 Potassium ChannelMiceNerve Tissue ProteinsTinnitusHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsKCNQ2 Potassium ChannelKcnq2 protein, mouseKCNQ3 Potassium ChannelKcnq3 protein, mouseNerve Tissue ProteinsHCN channelshomeostatic plasticityhyperexcitability-related disordersmouseneurosciencepotassium channelstinnitus

Identifiers

PMID26312501
PMCPMC4592936

What OpenQuestion holds

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Registered trials

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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.