Evidence map›Paper›PMID 9596797›Full record

ArticleThe Journal of physiology1998

Hypoxia activates ATP-dependent potassium channels in inspiratory neurones of neonatal mice.

S L Mironov, K Langohr, M Haller, D W Richter

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
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  9. Review
  10. The cellular building blocks of breathing.Comprehensive Physiology · 2012
    Review
  11. Fatal breathing dysfunction in a mouse model of Leigh syndrome.The Journal of clinical investigation · 2012
    Article
  12. Article
  13. Article
  14. Heme oxygenase is necessary for the excitatory response of cultured neonatal rat rostral ventrolateral medulla neurons to hypoxia.American journal of physiology. Regulatory, integrative and comparative physiology · 2009
    Article
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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

4 authors at 1 institution in 1 country.

S L MironovII Department of Physiology, University of Gottingen, Humboldtallee 23, Gottingen 37073, Germany.
K Langohr
M Haller
D W Richter
University of Göttingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. The respiratory centre of neonatal mice (4 to 12 days old) was isolated in 700 micro(m) thick brainstem slices. Whole-cell K+ currents and single ATP-dependent potassium (KATP) channels were analysed in inspiratory neurones. 2. In cell-attached patches, KATP channels had a conductance of 75 pS and showed inward rectification. Their gating was voltage dependent and channel activity decreased with membrane hyperpolarization. Using Ca2+-containing pipette solutions the measured conductance was lower (50 pS at 1.5 mM Ca2+), indicating tonic inhibition by extracellular Ca2+. 3. KATP channel activity was reversibly potentiated during hypoxia. Maximal effects were attained 3-4 min after oxygen removal from the bath. Hypoxic potentiation of open probability was due to an increase in channel open times and a decrease in channel closed times. 4. In inside-out patches and symmetrical K+ concentrations, channel currents reversed at about 0 mV. Channel activity was blocked by ATP (300-600 microM), glibenclamide (10-70 microM) and tolbutamide (100-300 microM). 5. In the presence of diazoxide (10-60 microM), the activity of KATP channels was increased both in inside-out, outside-out and cell-attached patches. In outside-out patches, that remained within the slice after excision, the activity of KATP channels was enhanced by hypoxia, an effect that could be mediated by a release of endogenous neuromodulators. 6. The whole-cell K+ current (IK) was inactivated at negative membrane potentials, which resembled the voltage dependence of KATP channel gating. After 3-4 min of hypoxia, K+ currents at both hyperpolarizing and depolarizing membrane potentials increased. IK was partially blocked by tolbutamide (100-300 microM) and in its presence, hypoxic potentiation of IK was abolished. 7. We conclude that KATP channels are involved in the hypoxic depression of medullary respiratory activity.

Indexed as

Adenosine TriphosphateAnimalsAnimals, NewbornCalciumDiazoxideElectric StimulationGlyburideHypoglycemic AgentsHypoxiaHypoxia, BrainIon Channel GatingMedulla OblongataMembrane PotentialsMiceNeuronsPatch-Clamp TechniquesAdenosine TriphosphateCalciumDiazoxideGlyburideHypoglycemic AgentsPotassium ChannelsTolbutamideVasodilator Agents

Identifiers

PMID9596797
PMCPMC2230998
OpenAlexW2120069128

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.