Evidence map›Paper›PMID 10704493›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000

Multiple G-protein betagamma combinations produce voltage-dependent inhibition of N-type calcium channels in rat superior cervical ganglion neurons.

V Ruiz-Velasco, S R Ikeda

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

26 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. GABAThe Journal of physiology · 2019
    Article
  5. Fast Inactivation of CaJournal of molecular neuroscience : MN · 2017
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. The molecular basis for T-type Ca2+ channel inhibition by G protein beta2gamma2 subunits.Proceedings of the National Academy of Sciences of the United States of America · 2006
    Article
  15. Gi protein activation in intact cells involves subunit rearrangement rather than dissociation.Proceedings of the National Academy of Sciences of the United States of America · 2003
    Article
  16. Neurotransmitter modulation of neuronal calcium channels.Journal of bioenergetics and biomembranes · 2003
    Review
  17. G-protein alpha subunit isoforms couple differentially to receptors that mediate presynaptic inhibition at rat hippocampal synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002
    Article
  18. Article
  19. GTP-binding protein beta gamma subunits mediate presynaptic calcium current inhibition by GABA(B) receptor.Proceedings of the National Academy of Sciences of the United States of America · 2001
    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.

V Ruiz-VelascoLaboratory of Molecular Physiology, Guthrie Research Institute, Sayre, Pennsylvania 18840, USA.
S R Ikeda
Guthrie Foundation · US

Funding

MOLECULAR MECHANISMS OF N TYPE CALCIUM CHANNEL MODULATIOR01GM056180 · NIGMS · GUTHRIE FOUNDATION FOR EDUCATION AND RES · PI IKEDA, STEPHEN R · 1997 to 2001
$485k
NIGMS NIH HHS GM 56180
6 · The paper itself

Abstract

Activation of several G-protein-coupled receptors leads to voltage-dependent (VD) inhibition of N- and P/Q-type Ca(2+) channels via G-protein betagamma subunits (Gbetagamma). The purpose of the present study was to determine the ability of different Gbetagamma combinations to produce VD inhibition of N-type Ca(2+) channels in rat superior cervical ganglion neurons. Various Gbetagamma combinations were heterologously overexpressed by intranuclear microinjection of cDNA and tonic VD Ca(2+) channel inhibition evaluated using the whole-cell voltage-clamp technique. Overexpression of Gbeta1-Gbeta5, in combination with several different Ggamma subunits, resulted in tonic VD Ca(2+) channel inhibition. Robust Ca(2+) channel modulation required coexpression of both Gbeta and Ggamma. Expression of either subunit alone produced minimal effects. To substantiate the apparent lack of Gbetagamma specificity, we examined whether heterologously expressed Gbetagamma displaced native Gbetagamma from heterotrimeric complexes. To this end, mutant Gbeta subunits were constructed that differentially modulated N-type Ca(2+) and G-protein-gated inward rectifier K(+) channels. Results from these studies indicated that significant displacement does not occur, and thus the observed Gbetagamma modulation can be attributed directly to the heterologously expressed Gbetagamma combinations.

Indexed as

GTP-Binding Protein beta SubunitsGTP-Binding Protein gamma SubunitsHeterotrimeric GTP-Binding ProteinsAnimalsCalcium Channels, N-TypeGene ExpressionGTP-Binding ProteinsIn Vitro TechniquesIon Channel GatingMaleMutagenesisNeural InhibitionNeuronsPatch-Clamp TechniquesPotassium ChannelsRatsCalcium Channels, N-TypeG-protein Beta gammaGTP-Binding Protein beta SubunitsGTP-Binding Protein gamma SubunitsGTP-Binding ProteinsHeterotrimeric GTP-Binding ProteinsPotassium Channels

Identifiers

PMID10704493
PMCPMC6772489
OpenAlexW1953015404

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.