Evidence map›Paper›PMID 8804605›Full record

ArticleBiophysical journal1996

A Ba2+ chelator suppresses long shut events in fully activated high-conductance Ca(2+)-dependent K+ channels.

J Neyton

Open access · bronzeAbstract read
In one paragraph

Article in Biophysical journal, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

22 citing papers in PubMed, 29 citations in OpenAlex.

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  5. Mg2+ enhances voltage sensor/gate coupling in BK channels.The Journal of general physiology · 2008
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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

1 author at 1 institution in 1 country.

J NeytonLaboratoire de Neurobiologie, Ecole Normale Supérieure, CNRS URA 1857, Paris, France. neyton@wotan.ens.fr
Laboratoire de Géologie de l’École Normale Supérieure · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High-conductance Ca(2+)-activated K+ channels from rat skeletal muscle were incorporated into planar lipid bilayers, and the channel kinetics were studied with a high internal Ca2+ concentration (Cai). Raising the Cai is known to increase the channel open probability. This effect is due to an increases in openings frequency and duration, and saturates at a Cai around 100 microM. Raising the Cai also increases the occurrence of less frequent but very long (> 5 s) shut events. The mechanism underlying this slow kinetic process was studied. Raising Cai above 100 microM does not further increase the frequency of the long shut events. This was not consistent with the hypothesis that the long closures result from a classical channel-block mechanism induced by internal Ca2+. The transmembrane voltage and the presence of K+ ions in the external compartment both affect the slow kinetic process. A comparison of these effects with the properties of the channel block induced by Ba2+ ions added to the internal compartment strongly suggested that the long shut events are due to a contamination of the internal solutions by Ba2+. This was confirmed by showing that a crown-ether compound that strongly chelates Ba2+ completely suppresses the long shut events when added to the inner compartment.

Indexed as

Crown EthersPotassium Channels, Calcium-ActivatedAnimalsBariumBiophysical PhenomenaBiophysicsCalciumChelating AgentsElectric ConductivityEthers, CyclicIn Vitro TechniquesKineticsLarge-Conductance Calcium-Activated Potassium ChannelsLipid BilayersMuscle, SkeletalPotassium Channels18-crown-6 2,3,11,12-tetracarboxylic acidBariumCalciumChelating AgentsCrown EthersEthers, CyclicLarge-Conductance Calcium-Activated Potassium ChannelsLipid BilayersPotassium ChannelsPotassium Channels, Calcium-Activated

Identifiers

PMID8804605
PMCPMC1233473
OpenAlexW1993579898

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.