Evidence map›Paper›PMID 16777937›Full record

ArticleThe Journal of physiology2006

KCNQ/M-currents contribute to the resting membrane potential in rat visceral sensory neurons.

Cynthia L Wladyka, Diana L Kunze

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

84 citing papers in PubMed, 135 citations in OpenAlex.

  1. Trial
  2. Article
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  4. Article
  5. Article
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  7. Article
  8. Article
  9. Article
  10. Glial KCNQ KNeuron · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. KCNQ Channels Enable Reliable Presynaptic Spiking and Synaptic Transmission at High Frequency.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  15. Article
  16. Article
  17. Chemical modulation of Kv7 potassium channels.RSC medicinal chemistry · 2021
    Review
  18. Article
  19. Review
  20. Article

24 more citing papers are in PubMed but not listed here.

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.

Cynthia L WladykaRammelkamp Centre for Research and Education R326 MetroHealth Medical Centre, 2500 MetroHealth Drive, Cleveland, OH 44109-1998, USA.
Diana L Kunze
MetroHealth · US

Funding

VENTROLATERAL PONS SHAPES THE RESPONSE TO HYPOXIAP01HL025830 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI PRABHAKAR, NANDURI R · 1985 to 2006
$11.1M
ION CHANNELS IN MECHANOSENSITIVE NEURONSR01HL061436 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI KUNZE, DIANA L · 1999 to 2007
$2.1M
NHLBI NIH HHS HL25830NHLBI NIH HHS HL61436NHLBI NIH HHS P01 HL025830NHLBI NIH HHS R01 HL061436
6 · The paper itself

Abstract

The M-current is a slowly activating, non-inactivating potassium current that has been shown to be present in numerous cell types. In this study, KCNQ2, Q3 and Q5, the molecular correlates of M-current in neurons, were identified in the visceral sensory neurons of the nodose ganglia from rats through immunocytochemical studies. All neurons showed expression of each of the three proteins. In voltage clamp studies, the cognition-enhancing drug linopirdine (1-50 microM) and its analogue, XE991 (10 microM), quickly and irreversibly blocked a small, slowly activating current that had kinetic properties similar to KCNQ/M-currents. This current activated between -60 and -55 mV, had a voltage-dependent activation time constant of 208 +/- 12 ms at -20 mV, a deactivation time constant of 165 +/- 24 ms at -50 mV and V1/2 of -24 +/- 2 mV, values which are consistent with previous reports for endogenous M-currents. In current clamp studies, these drugs also led to a depolarization of the resting membrane potential at values as negative as -60 mV. Flupirtine (10-20 microM), an M-current activator, caused a 3-14 mV leftward shift in the current-voltage relationship and also led to a hyperpolarization of resting membrane potential. These data indicate that the M-current is present in nodose neurons, is activated at resting membrane potential and that it is physiologically important in regulating excitability by maintaining cells at negative voltages.

Indexed as

AminopyridinesAnimalsAnthracenesCells, CulturedDose-Response Relationship, DrugIndolesKCNQ2 Potassium ChannelKCNQ3 Potassium ChannelKCNQ Potassium ChannelsMembrane PotentialsNeurons, AfferentNodose GanglionPotassiumPotassium Channel BlockersPyridinesRats10,10-bis(4-pyridinylmethyl)-9(10H)-anthracenoneAminopyridinesAnthracenesflupirtineIndolesKCNQ2 Potassium ChannelKcnq2 protein, ratKCNQ3 Potassium ChannelKcnq3 protein, ratKcnq5 protein, ratKCNQ Potassium ChannelslinopirdinePotassiumPotassium Channel BlockersPyridines

Identifiers

PMID16777937
PMCPMC1819429
OpenAlexW2128953287

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.