Evidence map›Paper›PMID 25447945›Full record

ArticleMolecular and cellular neurosciences2014

Modulation of CaV2.1 channels by neuronal calcium sensor-1 induces short-term synaptic facilitation.

Jin Yan, Karina Leal, Venkat G Magupalli, Evanthia Nanou, Gilbert Q Martinez, Todd Scheuer, William A Catterall

Abstract read
In one paragraph

Article in Molecular and cellular neurosciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

22 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Environmental Enrichment Enhances CaInternational journal of molecular sciences · 2021
    Article
  4. Neurotransmitter Release Site Replenishment and Presynaptic Plasticity.International journal of molecular sciences · 2020
    Review
  5. Review
  6. Article
  7. Review
  8. Presynaptic Calcium Channels.International journal of molecular sciences · 2019
    Review
  9. Calcium Sensors in Neuronal Function and Dysfunction.Cold Spring Harbor perspectives in biology · 2019
    Review
  10. Control of Excitation/Inhibition Balance in a Hippocampal Circuit by Calcium Sensor Protein Regulation of Presynaptic Calcium Channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Calcium sensor regulation of the CaV2.1 Ca2+ channel contributes to long-term potentiation and spatial learning.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  16. Article
  17. Article
  18. Article
  19. Calcium sensor regulation of the CaV2.1 Ca2+ channel contributes to short-term synaptic plasticity in hippocampal neurons.Proceedings of the National Academy of Sciences of the United States of America · 2016
    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

7 authors at 1 institution in 1 country.

Jin Yan
Karina Leal
Venkat G Magupalli
Evanthia Nanou
Gilbert Q Martinez
Todd Scheuer
William A Catterall
University of Washington · US

Funding

MOLECULAR PROPERTIES OF VOLTAGE-SENSITIVE CHANNELSR01NS022625 · NINDS · UNIVERSITY OF WASHINGTON · PI CATTERALL, WILLIAM A · 1985 to 2019
$6.2M
NINDS NIH HHS R01 NS022625NINDS NIH HHS R01-NS22625
6 · The paper itself

Abstract

Facilitation and inactivation of P/Q-type Ca2+ currents mediated by Ca2+/calmodulin binding to Ca(V)2.1 channels contribute to facilitation and rapid depression of synaptic transmission, respectively. Other calcium sensor proteins displace calmodulin from its binding site and differentially modulate P/Q-type Ca2 + currents, resulting in diverse patterns of short-term synaptic plasticity. Neuronal calcium sensor-1 (NCS-1, frequenin) has been shown to enhance synaptic facilitation, but the underlying mechanism is unclear. We report here that NCS-1 directly interacts with IQ-like motif and calmodulin-binding domain in the C-terminal domain of Ca(V)2.1 channel. NCS-1 reduces Ca2 +-dependent inactivation of P/Q-type Ca2+ current through interaction with the IQ-like motif and calmodulin-binding domain without affecting peak current or activation kinetics. Expression of NCS-1 in presynaptic superior cervical ganglion neurons has no effect on synaptic transmission, eliminating effects of this calcium sensor protein on endogenous N-type Ca2+ currents and the endogenous neurotransmitter release machinery. However, in superior cervical ganglion neurons expressing wild-type Ca(V)2.1 channels, co-expression of NCS-1 induces facilitation of synaptic transmission in response to paired pulses and trains of depolarizing stimuli, and this effect is lost in Ca(V)2.1 channels with mutations in the IQ-like motif and calmodulin-binding domain. These results reveal that NCS-1 directly modulates Ca(V)2.1 channels to induce short-term synaptic facilitation and further demonstrate that CaS proteins are crucial in fine-tuning short-term synaptic plasticity.

Indexed as

Synaptic TransmissionAmino Acid MotifsAnimalsBinding SitesCalcium Channels, N-TypeCells, CulturedHEK293 CellsHumansMiceNeuronal Calcium-Sensor ProteinsNeuropeptidesProtein BindingRatsSuperior Cervical GanglionSynapsesCalcium Channels, N-Typefrequenin calcium sensor proteinsNeuronal Calcium-Sensor ProteinsNeuropeptides

Identifiers

PMID25447945
PMCPMC4293345
OpenAlexW1965598205

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.