Evidence map›Paper›PMID 10908599›Full record

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

A voltage-independent calcium current inhibitory pathway activated by muscarinic agonists in rat sympathetic neurons requires both Galpha q/11 and Gbeta gamma.

P J Kammermeier, V Ruiz-Velasco, S R Ikeda

Open access · greenAbstract 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 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.7field-weighted citation impact, top 10% 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, 97 citations in OpenAlex.

  1. Article
  2. Review
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  4. Review
  5. Article
  6. Article
  7. Article
  8. Role of calcium channels in bipolar disorder.Current psychopharmacology · 2017
    Article
  9. Article
  10. Article
  11. Article
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  13. Phosphoinositides regulate ion channels.Biochimica et biophysica acta · 2015
    Review
  14. Article
  15. Article
  16. Review
  17. Article
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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 1 institution in 1 country.

P J KammermeierLaboratory of Molecular Physiology, Guthrie Research Institute, Sayre, PA 18840, USA.
V Ruiz-Velasco
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
PHYSIOLOGICAL ROLES OF METABOTROPIC GLUTAMATE RECEPTORSR01NS037615 · NINDS · GUTHRIE FOUNDATION FOR EDUCATION AND RES · PI IKEDA, STEPHEN R · 1997 to 2000
$238k
NIGMS NIH HHS GM56180NINDS NIH HHS NS10943NINDS NIH HHS NS37615
6 · The paper itself

Abstract

Calcium current modulation by the muscarinic cholinergic agonist oxotremorine methiodide (oxo-M) was examined in sympathetic neurons from the superior cervical ganglion of the rat. Oxo-M strongly inhibited calcium currents via voltage-dependent (VD) and voltage-independent (VI) pathways. These pathways could be separated with the use of the specific M(1) acetylcholine receptor antagonist M(1)-toxin and with pertussis toxin (PTX) treatment. Expression by nuclear cDNA injection of the regulator of G-protein signaling (RGS2) or a phospholipase Cbeta1 C-terminal construct (PLCbeta-ct) selectively reduced VI oxo-M modulation in PTX-treated and untreated cells. Expression of the Gbetagamma buffers transducin (Galpha(tr)) and a G-protein-coupled-receptor kinase (GRK3) construct (MAS-GRK3) eliminated oxo-M modulation. Activation of the heterologously expressed neurokinin type 1 receptor, a Galpha(q/11)-coupled receptor, resulted in VI calcium current modulation. This modulation was eliminated with coexpression of Galpha(tr) or MAS-GRK3. Cells expressing Gbeta(1)gamma(2) were tonically inhibited via the VD pathway. Application of oxo-M to these cells produced VI modulation and reduced the amount of current inhibited via the VD pathway. Together, these results confirm the requirement for Gbetagamma in VD modulation and implicate Galpha(q)-GTP and Gbetagamma as components in the potentially novel VI pathway.

Indexed as

GTP-Binding Protein beta SubunitsGTP-Binding Protein gamma SubunitsHeterotrimeric GTP-Binding ProteinsAnimalsBuffersCalciumCalcium Channels, N-TypeCells, CulturedElapid VenomsElectric StimulationElectrophysiologyGene ExpressionGenes, ReporterGreen Fluorescent ProteinsGTP-Binding Protein alpha Subunits, Gq-G11GTP-Binding ProteinsBuffersCalciumCalcium Channels, N-TypeElapid VenomsG-protein Beta gammaGreen Fluorescent ProteinsGTP-Binding Protein alpha Subunits, Gq-G11GTP-Binding Protein beta SubunitsGTP-Binding Protein gamma SubunitsGTP-Binding ProteinsHeterotrimeric GTP-Binding ProteinsIndicators and ReagentsIsoenzymesLuminescent Proteinsm1-toxinMuscarinic AgonistsMuscarinic AntagonistsNeurokinin-1 Receptor AntagonistsOxotremorineoxotremorine MPertussis ToxinPhospholipase C betaReceptors, Neurokinin-1Recombinant ProteinsRgs2 protein, mouseRGS ProteinsType C PhospholipasesVirulence Factors, Bordetella

Identifiers

PMID10908599
PMCPMC6772546
OpenAlexW2159306504

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.