Evidence map›Paper›PMID 11978818›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002

Isolation of a long-lasting eag-related gene-type K+ current in MMQ lactotrophs and its accommodating role during slow firing and prolactin release.

Marzia Lecchi, Elisa Redaelli, Barbara Rosati, Georgina Gurrola, Tullio Florio, Olivia Crociani, Giulia Curia, Rita Restano Cassulini, Alessio Masi, Annarosa Arcangeli and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.9field-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

15 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Scorpion venom components that affect ion-channels function.Toxicon : official journal of the International Society on Toxinology · 2013
    Review
  4. Review
  5. Erg K+ currents modulate excitability in mouse mitral/tufted neurons.Pflugers Archiv : European journal of physiology · 2009
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Therapeutic potential of venom peptides.Nature reviews. Drug discovery · 2003
    Review
  13. Article
  14. Article
  15. Review
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

14 authors at 5 institutions in 3 countries.

Marzia LecchiDepartment of Biotechnology and Biosciences, University of Milano-Bicocca, I-20126 Milano, Italy.
Elisa Redaelli
Barbara Rosati
Georgina Gurrola
Tullio Florio
Olivia Crociani
Giulia Curia
Rita Restano Cassulini
Alessio Masi
Annarosa Arcangeli
Massimo Olivotto
Gennaro Schettini
Lourival D Possani
Enzo Wanke
University of Milano-Bicocca · ITUniversity of Florence · ITUniversidad Nacional Autónoma de México · MXNational Cancer Research Institute · GBUniversity of Chieti-Pescara · IT

Funding

Telethon 1046
6 · The paper itself

Abstract

Native rat lactotrophs express thyrotrophin-releasing hormone-dependent K+ currents consisting of fast and slow deactivating components that are both sensitive to the class III anti-arrhythmic drugs that block the eag-related gene (ERG) K+ current (I(ERG)). Here we describe in MMQ prolactin-releasing pituitary cells the isolation of the slowly deactivating long-lasting component (I(ERGS)), which, unlike the fast component (I(ERGF)), is insensitive to verapamil 2 microm but sensitive to a novel scorpion toxin (ErgTx-2) that hardly affects I(ERGF). The time constants of I(ERGS) activation, deactivation, and recovery from inactivation are more than one order of magnitude greater than in I(ERGF), and the voltage-dependent inactivation is left-shifted by approximately 25 mV. The very slow MMQ firing frequency (approximately 0.2 Hz) investigated in perforated patch is increased approximately four times by anti-arrhythmic agents, by ErgTx-2, and by the abrupt I(ERGS) deactivation. Prolactin secretion in the presence of anti-arrhythmics is three- to fourfold higher in comparison with controls. We provide evidence from I(ERGS) and I(ERGF) simulations in a firing model cell to indicate that only I(ERGS) has an accommodating role during the experimentally observed very slow firing. Thus, we suggest that I(ERGS) potently modulates both firing and prolactin release in lactotroph cells.

Indexed as

Cation Transport ProteinsMembrane Transport ProteinsPotassium Channels, Voltage-GatedAction PotentialsAnimalsAnti-Arrhythmia AgentsBrainCalcium Channel BlockersCell LineComputer SimulationDose-Response Relationship, DrugERG1 Potassium ChannelEther-A-Go-Go Potassium ChannelsModels, NeurologicalPatch-Clamp TechniquesPituitary GlandAnti-Arrhythmia AgentsCalcium Channel BlockersCation Transport ProteinsERG1 Potassium ChannelEther-A-Go-Go Potassium ChannelsKCNH2 protein, humanKCNH6 protein, humanKcnh6 protein, ratKCNH7 protein, humanKcnh7 protein, ratMembrane Transport ProteinsPotassiumPotassium ChannelsPotassium Channels, Voltage-GatedProlactinRNAScorpion VenomsTretinoinVerapamil

Identifiers

PMID11978818
PMCPMC6758369
OpenAlexW1606051839

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.