Evidence map›Paper›PMID 11050179›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2000

Endogenous regulators of G protein signaling proteins regulate presynaptic inhibition at rat hippocampal synapses.

H Chen, N A Lambert

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Gain-of-function mutation in Gnao1: a murine model of epileptiform encephalopathy (EIEE17)?Mammalian genome : official journal of the International Mammalian Genome Society · 2014
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  10. Expression of Rem2, an RGK family small GTPase, reduces N-type calcium current without affecting channel surface density.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005
    Article
  11. Activation of NR2A-containing NMDA receptors is not obligatory for NMDA receptor-dependent long-term potentiation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005
    Article
  12. Article
  13. Article
  14. RGS3 mediates a calcium-dependent termination of G protein signaling in sensory neurons.Proceedings of the National Academy of Sciences of the United States of America · 2003
    Article
  15. Article
  16. 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
  17. Article
  18. 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.

H ChenDepartment of Pharmacology and Toxicology, Medical College of Georgia, and Medical Research Service, Veterans Affairs Medical Center, Augusta, GA 30912, USA.
N A Lambert
Augusta University · US

Funding

Regulation of G-protein signaling in CNS neuronsR01NS036455 · NINDS · MEDICAL COLLEGE OF GEORGIA (MCG) · PI LAMBERT, NEVIN ALAN · 2003 to 2006
$946k
MECHANISM OF FUNCTIONAL PRESYNAPTIC HETEROGENEITY IN CNSR29NS036455 · NINDS · MEDICAL COLLEGE OF GEORGIA (MCG) · PI LAMBERT, NEVIN ALAN · 1997 to 2001
$210k
NINDS NIH HHS NS36455NINDS NIH HHS R01 NS036455NINDS NIH HHS R29 NS036455
6 · The paper itself

Abstract

Presynaptic inhibition mediated by G protein-coupled receptors (GPCRs) can develop and decay in a few seconds. This time course is too rapid to be accounted for by the intrinsic GTPase activity of Galpha subunits alone. Here, we test the hypothesis that endogenous regulators of G protein signaling (RGS proteins) are required for rapid, brief presynaptic inhibition. Endogenous G protein alpha subunits were uncoupled from GPCRs by treating cultures with pertussis toxin (PTX). Adenoviral expression of mutant PTX-insensitive (PTX-i) Galpha(i1-3) or Galpha(o) subunits rescued adenosine-induced presynaptic inhibition in cultured hippocampal neurons. Expression of double mutant Galpha(i1) or Galpha(o) subunits that were both PTX-insensitive and unable to bind RGS proteins (PTX/RGS-i) also rescued presynaptic inhibition. Presynaptic inhibition mediated by PTX/RGS-i subunits decayed much more slowly after agonist removal than that mediated by PTX-i subunits or native G proteins. The onset of presynaptic inhibition mediated by PTX/RGS-i Galpha(o) was also slower than that mediated by PTX-i Galpha(o). In contrast, the onset of presynaptic inhibition mediated by PTX/RGS-i Galpha(i1) was similar to that mediated by PTX-i Galpha(i1). These results suggest that endogenous RGS proteins regulate the time course of G protein signaling in mammalian central nervous system presynaptic terminals.

Indexed as

AdenoviridaeAnimalsCells, CulturedGene ExpressionGenetic VectorsGTP-Binding Protein alpha Subunits, Gi-GoGTP-Binding Protein RegulatorsHeterotrimeric GTP-Binding ProteinsHippocampusNeural InhibitionNeuronsPertussis ToxinPresynaptic TerminalsRatsRecombinant Fusion ProteinsSignal TransductionGTP-Binding Protein alpha Subunits, Gi-GoGTP-Binding Protein RegulatorsHeterotrimeric GTP-Binding ProteinsPertussis ToxinRecombinant Fusion ProteinsVirulence Factors, Bordetella

Identifiers

PMID11050179
PMCPMC18846
OpenAlexW2088700210

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.