Evidence map›Paper›PMID 9634554›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998

Ca2+ channel beta3 subunit enhances voltage-dependent relief of G-protein inhibition induced by muscarinic receptor activation and Gbetagamma.

J P Roche, S N Treistman

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

13 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Origin of the voltage dependence of G-protein regulation of P/Q-type Ca2+ channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008
    Article
  3. Article
  4. Review
  5. Beta subunits of voltage-gated calcium channels.Journal of bioenergetics and biomembranes · 2003
    Review
  6. Article
  7. Ca2+-independent feedback inhibition of acetylcholine release in frog neuromuscular junction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Decreased G-protein-mediated regulation and shift in calcium channel types with age in hippocampal cultures.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999
    Article
  13. 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.

J P RocheDepartment of Pharmacology and Molecular Toxicology and Program in Neuroscience, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA.
S N Treistman
University of Massachusetts Chan Medical School · US

Funding

ALCOHOL ACTION ON NERVE TERMINALS IN SELECTED STRAINSR01AA008003 · NIAAA · WORCESTER FOUNDATION FOR BIOMEDICAL RES · PI TREISTMAN, STEVEN N · 1989 to 2009
$3.5M
IMPULSIVITY AND SEROTONIN AT RISK FOR TYPE II ALCOHOLISMF31AA005542 · NIAAA · ILLINOIS INSTITUTE OF TECHNOLOGY · PI CREAN, JOHN · 1999 to 2000
$26k
NIAAA NIH HHS AA05542NIAAA NIH HHS AA08003NIAAA NIH HHS F31 AA005542NIAAA NIH HHS R01 AA008003
6 · The paper itself

Abstract

The Ca2+ channel beta subunit has been shown to reduce the magnitude of G-protein inhibition of Ca2+ channels. However, neither the specificity of this action to different forms of G-protein inhibition nor the mechanism underlying this reduction in response is known. We have reported previously that coexpression of the Ca2+ channel beta3 subunit causes M2 muscarinic receptor-mediated inhibition of alpha1B Ca2+ currents to become more voltage-dependent. We report here that the beta3 subunit increases the rate of relief of inhibition produced by a depolarizing prepulse and also shifts the voltage dependency of this relief to more hyperpolarized voltages; these effects are likely to be responsible for the reduction of inhibitory response of alpha1B channels to G-protein-mediated inhibition seen after coexpression of the Ca2+ channel beta3 subunit. Additionally, the beta3 subunit alters the rate and voltage dependency of relief of the inhibition produced by coexpressed Gbeta1gamma1, in a manner similar to the changes it produces in relief of M2 receptor-induced inhibition. We conclude that the Ca2+ channel beta3 subunit reduces the magnitude of G-protein inhibition of alpha1B Ca2+ channels by enhancing the rate of dissociation of the G-protein betagamma subunit from the Ca2+ channel alpha1B subunit.

Indexed as

AcetylcholineAnimalsCalcium ChannelsEnzyme InhibitorsEthylmaleimideGene ExpressionGTP-Binding ProteinsIon Channel GatingOocytesReceptor, Muscarinic M2Receptors, MuscarinicTransfectionXenopusAcetylcholineCalcium ChannelsEnzyme InhibitorsEthylmaleimideGTP-Binding ProteinsReceptor, Muscarinic M2Receptors, Muscarinic

Identifiers

PMID9634554
PMCPMC6792574
OpenAlexW1944892775

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.