Evidence map›Paper›PMID 20219640›Full record

ArticleNeuroscience2010

Specific and rapid effects of acoustic stimulation on the tonotopic distribution of Kv3.1b potassium channels in the adult rat.

J G Strumbos, D B Polley, L K Kaczmarek

Abstract read
In one paragraph

Article in Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

29 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Frontiers in cellular neuroscience · 2026
    Article
  4. 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
  5. Modulation of potassium conductances optimizes fidelity of auditory information.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  6. Article
  7. Channelopathies in fragile X syndrome.Nature reviews. Neuroscience · 2021
    Review
  8. Review
  9. Single-nucleus RNA sequencing of mouse auditory cortex reveals critical period triggers and brakes.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  10. Mechanisms underlying auditory processing deficits in Fragile X syndrome.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Review
  11. Modulators of Kv3 Potassium Channels Rescue the Auditory Function of Fragile X Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  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 at 2 institutions in 1 country.

J G StrumbosDepartment of Pharmacology, Yale University School of Medicine, New Haven, CT 06511, USA.
D B Polley
L K Kaczmarek
Yale University · USVanderbilt University · US

Funding

EXPRESSION OF ION CHANNELS IN THE AUDITORY SYSTEMR01DC001919 · NIDCD · YALE UNIVERSITY · PI KACZMAREK, LEONARD K · 1993 to 2025
$9.7M
The Auditory Phenotype of Kv Channel Gene MutationsR03DC009488 · NIDCD · VANDERBILT UNIVERSITY · PI POLLEY, DANIEL B. · 2009 to 2011
$448k
NIDCD NIH HHS DC001919NIDCD NIH HHS DC009488NIDCD NIH HHS R01 DC001919NIDCD NIH HHS R03 DC009488
6 · The paper itself

Abstract

Recent studies have demonstrated that total cellular levels of voltage-gated potassium channel subunits can change on a time scale of minutes in acute slices and cultured neurons, raising the possibility that rapid changes in the abundance of channel proteins contribute to experience-dependent plasticity in vivo. In order to investigate this possibility, we took advantage of the medial nucleus of the trapezoid body (MNTB) sound localization circuit, which contains neurons that precisely phase-lock their action potentials to rapid temporal fluctuations in the acoustic waveform. Previous work has demonstrated that the ability of these neurons to follow high-frequency stimuli depends critically upon whether they express adequate amounts of the potassium channel subunit Kv3.1. To test the hypothesis that net amounts of Kv3.1 protein would be rapidly upregulated when animals are exposed to sounds that require high frequency firing for accurate encoding, we briefly exposed adult rats to acoustic environments that varied according to carrier frequency and amplitude modulation (AM) rate. Using an antibody directed at the cytoplasmic C-terminus of Kv3.1b (the adult splice isoform of Kv3.1), we found that total cellular levels of Kv3.1b protein-as well as the tonotopic distribution of Kv3.1b-labeled cells-was significantly altered following 30 min of exposure to rapidly modulated (400 Hz) sounds relative to slowly modulated (0-40 Hz, 60 Hz) sounds. These results provide direct evidence that net amounts of Kv3.1b protein can change on a time scale of minutes in response to stimulus-driven synaptic activity, permitting auditory neurons to actively adapt their complement of ion channels to changes in the acoustic environment.

Indexed as

Acoustic StimulationAdaptation, PhysiologicalAnimalsAntibody SpecificityAuditory PathwaysAuditory ThresholdImmunohistochemistryIon Channel GatingNerve Tissue ProteinsNeuronal PlasticityRatsRats, Sprague-DawleyReaction TimeRhombencephalonShaw Potassium ChannelsSound LocalizationKcnc1 protein, ratNerve Tissue ProteinsShaw Potassium Channels

Identifiers

PMID20219640
PMCPMC2854512
OpenAlexW1988415122

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.