Evidence map›Paper›PMID 17267561›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007

Drosophila cacophony channels: a major mediator of neuronal Ca2+ currents and a trigger for K+ channel homeostatic regulation.

I-Feng Peng, Chun-Fang Wu

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

40 citing papers in PubMed, 62 citations in OpenAlex.

  1. CaeLife · 2024
    Article
  2. CabioRxiv : the preprint server for biology · 2024
    Article
  3. Article
  4. Endogenous Tagging Reveals Differential Regulation of CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  5. Article
  6. Restoration of Olfactory Memory inFrontiers in cellular neuroscience · 2019
    Article
  7. Dissecting Motor Neuron Disease WithFrontiers in neuroscience · 2019
    Review
  8. Article
  9. Conservation of cardiac L-type CaJournal of molecular and cellular cardiology · 2018
    Article
  10. Article
  11. Article
  12. Restoration of Motor Defects Caused by Loss ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  13. Nonreciprocal homeostatic compensation inJournal of neurophysiology · 2017
    Article
  14. Spontaneous CaFrontiers in molecular neuroscience · 2017
    Article
  15. Article
  16. Review
  17. 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

2 authors at 1 institution in 1 country.

I-Feng PengDepartment of Biological Sciences, University of Iowa, Iowa City, Iowa 52242, USA.
Chun-Fang Wu
University of Iowa · US

Funding

VIDEO LABORATORY FOR ANALYSIS OF CELL BEHAVIORP01HD018577 · NICHD · UNIVERSITY OF IOWA · PI VOSS, EDWARD R · 1985 to 2006
$5.1M
Plasticity of Neuronal Function and Form in DrosophilaR01NS026528 · NINDS · UNIVERSITY OF IOWA · PI WU, CHUN-FANG · 1988 to 2007
$2.0M
NICHD NIH HHS HD18577NICHD NIH HHS P01 HD018577NINDS NIH HHS NS26528NINDS NIH HHS R01 NS026528
6 · The paper itself

Abstract

The cacophony (cac) locus in Drosophila encodes a Ca2+ channel alpha subunit, but little is known about properties of cac-mediated currents and functional consequences of cac mutations in central neurons. We found that, in Drosophila cultured neurons, Ca2+ currents were mediated predominantly by the cac channels. The cac channels contribute to low- and high-threshold, fast- and slow-inactivating types of Ca2+ currents, take part in membrane depolarization, and strongly activate Ca2+-activated K+ current [I(K(Ca))]. In cac neurons, unexpectedly, voltage-activated transient K+ current I(A) is upregulated to a level that matches I(K(Ca)) reduction, implicating a homeostatic regulation that was mimicked by chronic pharmacological blockade of Ca2+ currents in wild-type neurons. Among K+ channel transcripts, Shaker mRNA levels were preferentially increased in cac flies. However, Ca2+ current expression levels remained unaltered in several K+ channel mutants, illustrating a key role of cac in developmental regulation of Drosophila neuronal excitability.

Indexed as

AnimalsCalcium ChannelsCells, CulturedDrosophilaDrosophila ProteinsHomeostasisNeuronsPotassium Channelscac protein, DrosophilaCalcium ChannelsDrosophila ProteinsPotassium Channels

Identifiers

PMID17267561
PMCPMC6673189
OpenAlexW2091649989

What OpenQuestion holds

Textmetadata
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.