Evidence map›Paper›PMID 16148236›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005

Developmental activation of calmodulin-dependent facilitation of cerebellar P-type Ca2+ current.

Dipayan Chaudhuri, Badr A Alseikhan, Siao Yun Chang, Tuck Wah Soong, David T Yue

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.5field-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

37 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Presynaptic Calcium Channels.International journal of molecular sciences · 2019
    Review
  7. The Role of CaCell reports · 2019
    Article
  8. Splicing of an automodulatory domain in CaThe Journal of general physiology · 2018
    Article
  9. A bilobal model of CaThe Journal of general physiology · 2018
    Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Genetic, cellular, and functional evidence for Ca2+ inflow through Cav1.2 and Cav1.3 channels in murine spiral ganglion neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  16. Article
  17. Article
  18. Ca²⁺-dependent regulation of Ca²⁺ currents in rat primary afferent neurons: role of CaMKII and the effect of injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  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

5 authors at 3 institutions in 2 countries.

Dipayan ChaudhuriDepartment of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
Badr A Alseikhan
Siao Yun Chang
Tuck Wah Soong
David T Yue
Johns Hopkins Medicine · USNational University of Singapore · SGJohns Hopkins University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

P-type (CaV2.1) Ca2+ channels are a central conduit of neuronal Ca2+ entry, so their Ca2+ feedback regulation promises widespread neurobiological impact. Heterologous expression of recombinant CaV2.1 channels demonstrates that the Ca2+ sensor calmodulin can trigger Ca2+-dependent facilitation (CDF) of channel opening. This facilitation occurs when local Ca2+ influx through individual channels selectively activates the C-terminal lobe of calmodulin. In neurons, however, such calmodulin-mediated processes have yet to be detected, and CDF of native P-type current has thus far appeared different, arguably triggered by other Ca2+ sensing molecules. Here, in cerebellar Purkinje somata abundant with prototypic P-type channels, we find that the C-terminal lobe of calmodulin does produce CDF, and such facilitation augments Ca2+ entry during stimulation by repetitive action-potential and complex-spike waveforms. Beyond recapitulating key features of recombinant channels, these neurons exhibit an additional modulatory dimension: developmental upregulation of CDF during postnatal week 2. This phenomenon reflects increasing somatic expression of CaV2.1 splice variants that manifest CDF and progressive dendritic targeting of variants lacking CDF. Calmodulin-triggered facilitation is thus fundamental to native CaV2.1 and rapidly enhanced during early development.

Indexed as

AnimalsCalcium Channel BlockersCalcium Channels, P-TypeCalmodulinCell LineCerebellumHumansKidneyNimodipinePlasmidsPurkinje CellsRatsRats, Sprague-DawleyTetrodotoxinTransfectionCalcium Channel BlockersCalcium Channels, P-TypeCalmodulinNimodipineTetrodotoxin

Identifiers

PMID16148236
PMCPMC6725527
OpenAlexW1992096875

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.