Evidence map›Paper›PMID 16636868›Full record

ArticlePflugers Archiv : European journal of physiology2006

On the functional interaction between nicotinic acetylcholine receptor and Na+,K+-ATPase.

Igor I Krivoi, Tatiana M Drabkina, Violetta V Kravtsova, Alexander N Vasiliev, Misty J Eaton, Serguei N Skatchkov, Frederic Mandel

Abstract read
PubMed Publisher
In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

27 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. The role of AMPK in regulation of NaJournal of muscle research and cell motility · 2021
    Review
  8. Article
  9. Article
  10. Skeletal Muscle Na,K-ATPase as a Target for Circulating Ouabain.International journal of molecular sciences · 2020
    Article
  11. Article
  12. Cholesterol and the Safety Factor for Neuromuscular Transmission.International journal of molecular sciences · 2019
    Review
  13. NaInvertebrate neuroscience : IN · 2018
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Presynaptic neuromuscular action of a methanolic extract from the venom of Rhinella schneideri toad.The journal of venomous animals and toxins including tropical diseases · 2014
    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

7 authors at 3 institutions in 3 countries.

Igor I KrivoiDepartment of General Physiology, St. Petersburg State University, 7/9 University emb., St. Petersburg 199034, Russia. IgorKrivoi@IK4251.spb.edu
Tatiana M Drabkina
Violetta V Kravtsova
Alexander N Vasiliev
Misty J Eaton
Serguei N Skatchkov
Frederic Mandel
St Petersburg University · RUCentral University of the Caribbean · PRUniversity of Cincinnati Medical Center · US

Funding

UNIVERSITY MEDICAL RESEARCH CENTERG12RR003035 · NCRR · UNIVERSIDAD CENTRAL DEL CARIBE · PI ROJAS, LEGIER V · 1986 to 2011
$26.7M
Synaptic Remodeling and Thyroid HormonesS06GM050695 · NIGMS · UNIVERSIDAD CENTRAL DEL CARIBE · PI CUBANO, LUIS ANGEL · 1994 to 2009
$10.7M
NCRR NIH HHS G12 RR 03035NIGMS NIH HHS S06 GM 50695
6 · The paper itself

Abstract

Previous studies have shown that nanomolar acetylcholine (ACh) produces a 2 to 4-mV hyperpolarization of skeletal muscle fibers putatively due to Na(+),K(+)-ATPase activation. The present study elucidates the involvement of the nicotinic ACh receptor (nAChR) and of Na(+),K(+)-ATPase isoform(s) in ACh-induced hyperpolarization of rat diaphragm muscle fibers. A variety of ligands of specific binding sites of nAChR and Na(+),K(+)-ATPase were used. Dose-response curves for ouabain, a specific Na(+),K(+)-ATPase inhibitor, were obtained to ascertain which Na(+),K(+)-ATPase isoform(s) is involved. The ACh dose-response relationship for the hyperpolarization was also determined. The functional relationship between these two proteins was also studied in a less complex system, a membrane preparation from Torpedo electric organ. The possibility of a direct ACh effect on Na(+),K(+)-ATPase was studied in purified lamb kidney Na(+),K(+)-ATPase and in rat red blood cells, systems where no nAChR is present. The results indicate that binding of nAChR agonists to their specific sites results in modulation of ouabain-sensitive (most probably alpha2) isoform of Na(+),K(+)-ATPase, leading to muscle membrane hyperpolarization. In the Torpedo preparation, ouabain modulates dansyl-C6-choline binding to nAChR, and vice versa. These results provide the first evidence of a functional interaction between nAChR and Na(+),K(+)-ATPase. Possible interaction mechanisms are discussed.

Indexed as

AcetylcholineAnimalsCell MembraneDansyl CompoundsEnzyme InhibitorsErythrocyte MembraneIn Vitro TechniquesMaleMuscle Fibers, SkeletalMuscle, SkeletalNicotineNicotinic AgonistsOuabainQuaternary Ammonium CompoundsRatsRats, Wistar(1-(5-dimethylaminonaphthalene)sulfonamido)-n-hexanoic acid-beta-N-trimethylammonium ethyl esterAcetylcholineAtp1a2 protein, ratDansyl CompoundsEnzyme InhibitorsNicotineNicotinic AgonistsOuabainQuaternary Ammonium CompoundsReceptors, NicotinicSodium-Potassium-Exchanging ATPase

Identifiers

PMID16636868
OpenAlexW2075810805

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.