Evidence map›Paper›PMID 17627990›Full record

ArticleThe Journal of physiology2007

Genetic deletion of SK2 channels in mouse inner hair cells prevents the developmental linearization in the Ca2+ dependence of exocytosis.

Stuart L Johnson, John P Adelman, Walter Marcotti

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2007. 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
1.5field-weighted citation impact, top 18% 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

43 citing papers in PubMed, 56 citations in OpenAlex.

  1. Spontaneous Calcium Signalling in the Developing Mammalian Cochlea.Journal of the Association for Research in Otolaryngology : JARO · 2026
    Review
  2. Article
  3. Review
  4. Auditory hair cells and spiral ganglion neurons regenerate synapses with refined release properties in vitro.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Fast CaFrontiers in molecular neuroscience · 2018
    Article
  12. The Coupling between CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  13. Absence of Neuroplastin-65 Affects Synaptogenesis in Mouse Inner Hair Cells and Causes Profound Hearing Loss.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  14. Review
  15. Review
  16. Article
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  18. Article
  19. Spatiotemporal pattern of action potential firing in developing inner hair cells of the mouse cochlea.Proceedings of the National Academy of Sciences of the United States of America · 2014
    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 at 2 institutions in 2 countries.

Stuart L JohnsonDepartment of Biomedical Science, University of Sheffield, Sheffield S10 2TN, UK.
John P Adelman
Walter Marcotti
University of Sheffield · GBOregon Health & Science University · US

Funding

Wellcome Trust
6 · The paper itself

Abstract

Inner hair cells (IHCs), the primary sensory receptors of the mammalian cochlea, fire spontaneous Ca(2+) action potentials (APs) only before the onset of hearing. Although a role for APs in the developing auditory system has not been determined it could, by analogy with other sensory systems, guide the functional maturation of the cochlea before experience-driven activity begins. Spontaneous APs in immature IHCs are shaped by a variety of ion channels including that of the small conductance Ca(2+)-activated K(+) current (SK2), which is only transiently expressed in immature cells. Using SK2 knockout mice we found that SK2 channels are not required for generating APs but are essential for sustaining continuous repetitive spontaneous AP activity in pre-hearing IHCs. Therefore we used this mutant mouse as a model to study possible developmental implications of disrupted AP activity. Immature mutant IHCs showed impaired exocytotic responses, which are likely to be due to the expression of fewer Ca(2+) channels. Exocytosis was also impaired in adult mutant IHCs, although in this case it resulted from a reduced Ca(2+) efficiency and increased Ca(2+) dependence of the synaptic machinery. Since SK2 channels can only have a functional influence on IHCs during immature development and are not directly involved in neurotransmitter release, the altered Ca(2+) dependence of exocytosis in adult IHCs is likely to be a consequence of their disrupted AP activity at immature stages.

Indexed as

Calcium SignalingExocytosisAction PotentialsAgingAnimalsCochleaElectric CapacitanceHair Cells, Auditory, InnerMiceMice, KnockoutPotassiumSmall-Conductance Calcium-Activated Potassium ChannelsTime FactorsKcnn2 protein, mousePotassiumSmall-Conductance Calcium-Activated Potassium Channels

Identifiers

PMID17627990
PMCPMC2096744
OpenAlexW2141285799

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.