Evidence map›Paper›PMID 26950800›Full record

ArticleChannels (Austin, Tex.)2016

Assessing the role of IKCa channels in generating the sAHP of CA1 hippocampal pyramidal cells.

Ray W Turner, Hadhimulya Asmara, Jordan D T Engbers, Jason Miclat, Arsalan P Rizwan, Giriraj Sahu, Gerald W Zamponi

Abstract read
In one paragraph

Article in Channels (Austin, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Article
  2. Review
  3. Calcium-Dependent Regulation of Neuronal Excitability Is Rescued in Fragile X Syndrome by a Tat-Conjugated N-Terminal Fragment of FMRP.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  4. Article
  5. Corticotropin Releasing Factor Mediates KThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  6. Article
  7. Ion Channels in Glioma Malignancy.Reviews of physiology, biochemistry and pharmacology · 2021
    Review
  8. Review
  9. CaScientific reports · 2020
    Article
  10. Review
  11. Protein Kinase A-Mediated Suppression of the Slow Afterhyperpolarizing KCa3.1 Current in Temporal Lobe Epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  12. Review
  13. βJournal of neurophysiology · 2019
    Article
  14. Article
  15. Activity-Dependent Facilitation of CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  16. Article
  17. Article
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

7 authors.

Ray W Turnera Hotchkiss Brain Institute, University of Calgary , Calgary , AB , Canada.
Hadhimulya Asmaraa Hotchkiss Brain Institute, University of Calgary , Calgary , AB , Canada.
Jordan D T Engbersa Hotchkiss Brain Institute, University of Calgary , Calgary , AB , Canada.
Jason Miclata Hotchkiss Brain Institute, University of Calgary , Calgary , AB , Canada.
Arsalan P Rizwana Hotchkiss Brain Institute, University of Calgary , Calgary , AB , Canada.
Giriraj Sahua Hotchkiss Brain Institute, University of Calgary , Calgary , AB , Canada.
Gerald W Zamponia Hotchkiss Brain Institute, University of Calgary , Calgary , AB , Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our previous work reported that KCa3.1 (IKCa) channels are expressed in CA1 hippocampal pyramidal cells and contribute to the slow afterhyperpolarization that regulates spike accommodation in these cells. The current report presents data from single cell RT-PCR that further reveals mRNA in CA1 cells that corresponds to the sequence of an IKCa channel from transmembrane segments 5 through 6 including the pore region, revealing the established binding sites for 4 different IKCa channel blockers. A comparison of methods to internally apply the IKCa channel blocker TRAM-34 shows that including the drug in an electrode from the onset of an experiment is unviable given the speed of drug action upon gaining access for whole-cell recordings. Together the data firmly establish IKCa channel expression in CA1 neurons and clarify methodological requirements to obtain a block of IKCa channel activity through internal application of TRAM-34.

Indexed as

AnimalsCA1 Region, HippocampalIntermediate-Conductance Calcium-Activated Potassium ChannelsMaleMembrane PotentialsPatch-Clamp TechniquesPolymerase Chain ReactionPotassium Channel BlockersPyramidal CellsPyrazolesRatsRats, Sprague-DawleyRNA, MessengerIntermediate-Conductance Calcium-Activated Potassium ChannelsKcnn4 protein, ratPotassium Channel BlockersPyrazolesRNA, MessengerTRAM 34CA1 pyramidalIKCasAHPslow AHPTRAM-34

Identifiers

PMID26950800
PMCPMC4954577

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.