Evidence map›Paper›PMID 11466425›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001

Activation of expressed KCNQ potassium currents and native neuronal M-type potassium currents by the anti-convulsant drug retigabine.

L Tatulian, P Delmas, F C Abogadie, D A Brown

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 189 papers.

0numbers the graph read from it
0cells of the map it votes in
189citing papers in PubMed
–field-weighted citation impact
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

189 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Plural molecular and cellular mechanisms of pore domainbioRxiv : the preprint server for biology · 2024
    Article
  10. Glial KCNQ KNeuron · 2024
    Article
  11. Article
  12. Identifying the mechanism of action of the Kv7 channel opener, retigabine in the treatment of epilepsy.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023
    Review
  13. Article
  14. Article
  15. Overlooked KCNQ4 variants augment the risk of hearing loss.Experimental & molecular medicine · 2023
    Article
  16. A Role for KCNQ Channels on Cell Type-Specific Plasticity in Mouse Auditory Cortex after Peripheral Damage.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  17. Article
  18. Article
  19. Article
  20. Article

129 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

4 authors.

L TatulianDepartment of Pharmacology and Wellcome Laboratory for Molecular Pharmacology, University College London, London WC1E 6BT, United Kingdom.
P Delmas
F C Abogadie
D A Brown

Funding

Wellcome Trust
6 · The paper itself

Abstract

Retigabine [D-23129; N-(2-amino-4-(4-fluorobenzylamino)-phenyl) carbamic acid ethyl ester] is a novel anticonvulsant compound that is now in clinical phase II development. It has previously been shown to enhance currents generated by KCNQ2/3 K(+) channels when expressed in Chinese hamster ovary (CHO) cells (Main et al., 2000; Wickenden et al., 2000). In the present study, we have compared the actions of retigabine on KCNQ2/3 currents with those on currents generated by other members of the KCNQ family (homomeric KCNQ1, KCNQ2, KCNQ3, and KCNQ4 channels) expressed in CHO cells and on the native M current in rat sympathetic neurons [thought to be generated by KCNQ2/3 channels (Wang et al., 1998)]. Retigabine produced a hyperpolarizing shift of the activation curves for KCNQ2/3, KCNQ2, KCNQ3, and KCNQ4 currents with differential potencies in the following order: KCNQ3 > KCNQ2/3 > KCNQ2 > KCNQ4, as measured either by the maximum hyperpolarizing shift in the activation curves or by the EC(50) values. In contrast, retigabine did not enhance cardiac KCNQ1 currents. Retigabine also produced a hyperpolarizing shift in the activation curve for native M channels in rat sympathetic neurons. The retigabine-induced current was inhibited by muscarinic receptor stimulation, with similar agonist potency but 25% reduced maximum effect. In unclamped neurons, retigabine produced a hyperpolarization and reduced the number of action potentials produced by depolarizing current injections, without change in action potential configuration.

Indexed as

Potassium Channels, Voltage-GatedAction PotentialsAnimalsAnticonvulsantsCarbamatesCells, CulturedCHO CellsCricetinaeHumansIndolesIon TransportKCNQ1 Potassium ChannelKCNQ2 Potassium ChannelKCNQ3 Potassium ChannelKCNQ Potassium ChannelsMuscarinic AgonistsAnticonvulsantsCarbamatesezogabineIndolesKCNQ1 Potassium ChannelKCNQ1 protein, humanKcnq1 protein, ratKCNQ2 Potassium ChannelKCNQ2 protein, humanKcnq2 protein, ratKCNQ3 Potassium ChannelKCNQ3 protein, humanKcnq3 protein, ratKCNQ4 protein, humanKcnq4 protein, ratKCNQ Potassium ChannelslinopirdineMuscarinic AgonistsPhenylenediaminesPotassiumPotassium ChannelsPotassium Channels, Voltage-GatedPyridinesReceptor, Muscarinic M1Receptors, Muscarinic

Identifiers

PMID11466425
PMCPMC6762632

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.