Evidence map›Paper›PMID 24920626›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

Role of small conductance Ca²⁺-activated K⁺ channels in controlling CA1 pyramidal cell excitability.

Shmuel Chen, Felix Benninger, Yoel Yaari

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 56 citations in OpenAlex.

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  7. Implications of Oligomeric Amyloid-Beta (oAβThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
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  14. Regulation of Neuronal NaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  15. βJournal of neurophysiology · 2019
    Article
  16. Intrinsic Mechanisms of Frequency Selectivity in the Proximal Dendrites of CA1 Pyramidal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  17. Article
  18. Article
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  20. Activity-Dependent Facilitation of CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    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

3 authors at 1 institution in 1 country.

Shmuel ChenDepartment of Medical Neurobiology, Institute for Medical Research Israel-Canada, Hebrew University-Hadassah School of Medicine, Jerusalem 91120, Israel.ORCID http://orcid.org/0000-0001-8843-1777
Felix BenningerDepartment of Medical Neurobiology, Institute for Medical Research Israel-Canada, Hebrew University-Hadassah School of Medicine, Jerusalem 91120, Israel.ORCID http://orcid.org/0000-0003-3097-4693
Yoel YaariDepartment of Medical Neurobiology, Institute for Medical Research Israel-Canada, Hebrew University-Hadassah School of Medicine, Jerusalem 91120, Israel yaari@md.huji.ac.il.
Hebrew University of Jerusalem · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Small-conductance Ca(2+)-activated K(+) (SK or K(Ca)2) channels are widely expressed in the CNS. In several types of neurons, these channels were shown to become activated during repetitive firing, causing early spike frequency adaptation. In CA1 pyramidal cells, SK channels in dendritic spines were shown to regulate synaptic transmission. However, the presence of functional SK channels in the somata and their role in controlling the intrinsic firing of these neurons has been controversial. Using whole-cell voltage-clamp and current-clamp recordings in acute hippocampal slices and focal applications of irreversible and reversible SK channel blockers, we provide evidence that functional SK channels are expressed in the somata and proximal dendrites of adult rat CA1 pyramidal cells. Although these channels can generate a medium duration afterhyperpolarizing current, they play only an auxiliary role in controlling the intrinsic excitability of these neurons, secondary to the low voltage-activating, noninactivating K(V)7/M channels. As long as K(V)7/M channels are operative, activation of SK channels during repetitive firing does not notably affect the spike output of CA1 pyramidal cells. However, when K(V)7/M channel activity is compromised, SK channel activation significantly and uniquely reduces spike output of these neurons. Therefore, proximal SK channels provide a "second line of defense" against intrinsic hyperexcitability, which may play a role in multiple conditions in which K(V)7/M channels activity is compromised, such as hyposmolarity.

Indexed as

4-AminopyridineAction PotentialsAnalysis of VarianceAnimalsAnthracenesApaminBiophysicsCA1 Region, HippocampalDendritesElectric StimulationIn Vitro TechniquesMalePatch-Clamp TechniquesPotassium Channel BlockersPotassium ChloridePyramidal Cells10,10-bis(4-pyridinylmethyl)-9(10H)-anthracenone4-AminopyridineAnthracenesApaminPotassium Channel BlockersPotassium ChlorideSmall-Conductance Calcium-Activated Potassium ChannelsBurstinghippocampusKv7 channelsmAHPpyramidal cellSK channels

Identifiers

PMID24920626
PMCPMC6608239
OpenAlexW2067722760

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.