Evidence map›Paper›PMID 9490860›Full record

ArticleThe Journal of physiology1998

On the role of endogenous G-protein beta gamma subunits in N-type Ca2+ current inhibition by neurotransmitters in rat sympathetic neurones.

P Delmas, D A Brown, M Dayrell, F C Abogadie, M P Caulfield, N J Buckley

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 77 citations in OpenAlex.

  1. Fast Inactivation of CaJournal of molecular neuroscience : MN · 2017
    Article
  2. Nerve growth factor sensitizes adult sympathetic neurons to the proinflammatory peptide bradykinin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
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  9. Neurotransmitter modulation of neuronal calcium channels.Journal of bioenergetics and biomembranes · 2003
    Review
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  17. Activation of expressed KCNQ potassium currents and native neuronal M-type potassium currents by the anti-convulsant drug retigabine.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001
    Article
  18. 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
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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

6 authors at 2 institutions in 1 country.

P DelmasWellcome Laboratory for Molecular Pharmacology, Department of Pharmacology, University College London, UK. ucklpds@ucl.ac.uk
D A Brown
M Dayrell
F C Abogadie
M P Caulfield
N J Buckley
University College London · GBNinewells Hospital · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

1. Using whole-cell and perforated-patch recordings, we have examined the part played by endogenous G-protein beta gamma subunits in neurotransmitter-mediated inhibition of N-type Ca2+ channel current (ICa) in dissociated rat superior cervical sympathetic neurones. 2. Expression of the C-terminus domain of beta-adrenergic receptor kinase 1 (beta ARK1), which contains the consensus motif (QXXER) for binding G beta gamma, reduced the fast (pertussis toxin (PTX)-sensitive) and voltage-dependent inhibition of ICa by noradrenaline and somatostatin, but not the slow (PTX-insensitive) and voltage-independent inhibition induced by angiotensin II. beta ARK1 peptide reduced GTP-gamma-S-induced voltage-dependent and PTX-sensitive inhibition of ICa but not GTP-gamma-S-mediated voltage-independent inhibition. 3. Overexpression of G beta 1 gamma 2, which mimicked the voltage-dependent inhibition by reducing ICa density and enhancing basal facilitation, occluded the voltage-dependent noradrenaline- and somatostatin-mediated inhibitions but not the inhibition mediated by angiotensin II. 4. Co-expression of the C-terminus of beta ARK1 with beta 1 and gamma 2 subunits prevented the effects of G beta gamma dimers on basal Ca2+ channel behaviour in a manner consistent with the sequestering of G beta gamma. 5. The expression of the C-terminus of beta ARK1 slowed down reinhibition kinetics of ICa following conditioning depolarizations and induced long-lasting facilitation by cumulatively sequestering beta gamma subunits. 6. Our findings identify endogenous G beta gamma as the mediator of the voltage-dependent, PTX-sensitive inhibition of ICa induced by both noradrenaline and somatostatin but not the voltage-independent. PTX-insensitive inhibition by angiotensin II. They also support the view that voltage-dependent inhibition results from a direct G beta gamma-Ca2+ channel interaction.

Indexed as

Angiotensin IIAnimalsbeta-Adrenergic Receptor KinasesCalcium ChannelsCyclic AMP-Dependent Protein KinasesElectrophysiologyGene ExpressionGTP-Binding ProteinsGuanosine 5'-O-(3-Thiotriphosphate)HumansIon Channel GatingKineticsNeuronsNeurotransmitter AgentsNorepinephrinePertussis ToxinAngiotensin IIbeta-Adrenergic Receptor KinasesCalcium ChannelsCyclic AMP-Dependent Protein KinasesGTP-Binding ProteinsGuanosine 5'-O-(3-Thiotriphosphate)Neurotransmitter AgentsNorepinephrinePertussis ToxinReceptors, Adrenergic, alphaReceptors, SomatostatinRecombinant ProteinsSomatostatinVirulence Factors, Bordetella

Identifiers

PMID9490860
PMCPMC2230730
OpenAlexW2088650169

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.