Evidence map›Paper›PMID 15190101›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004

Small conductance Ca2+-activated K+ channel knock-out mice reveal the identity of calcium-dependent afterhyperpolarization currents.

Chris T Bond, Paco S Herson, Timothy Strassmaier, Rebecca Hammond, Robert Stackman, James Maylie, John P Adelman

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 papers.

0numbers the graph read from it
0cells of the map it votes in
158citing papers in PubMed
7.3field-weighted citation impact, top 1% 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

158 citing papers in PubMed, 291 citations in OpenAlex.

  1. Article
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  11. CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  12. Article
  13. Article
  14. The small conductance CaNeuropharmacology · 2024
    Article
  15. Article
  16. Article
  17. Article
  18. KJournal of neuroscience research · 2023
    Review
  19. A NovelGenes · 2023
    Article
  20. Article

98 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

7 authors at 1 institution in 1 country.

Chris T BondVollum Institute, Oregon Health and Science University, Portland, Oregon 97239, USA.
Paco S Herson
Timothy Strassmaier
Rebecca Hammond
Robert Stackman
James Maylie
John P Adelman
Oregon Health & Science University · US

Funding

Molecular Physiology of the SK2 Channels in CA1 NeuronsR01NS038880 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI MAYLIE, JAMES G · 2000 to 2017
$6.0M
Activity Dependent Modulation of SK2 ChannelsF32MH080480 · NIMH · OREGON HEALTH & SCIENCE UNIVERSITY · PI LIN, MIKE T · 2008 to 2009
$105k
NIMH NIH HHS F32 MH080480NINDS NIH HHS NS38880NINDS NIH HHS R01 NS038880
6 · The paper itself

Abstract

Action potentials in many central neurons are followed by a prolonged afterhyperpolarization (AHP) that influences firing frequency and affects neuronal integration. In hippocampal CA1 pyramidal neurons, the current ascribed to the AHP (IAHP) has three kinetic components. The IfastAHP is predominantly attributable to voltage-dependent K+ channels, whereas Ca2+-dependent and voltage-independent K+channels contribute to the ImediumAHP (ImAHP) and IslowAHP (IsAHP). Apamin, which selectively suppresses a component of the mAHP, increases neuronal excitability and facilitates the induction of synaptic plasticity at Schaffer collateral synapses and hippocampal-dependent learning. The Ca2+-dependent components of the AHP have been attributed to the activity of small conductance Ca2+-activated K+ (SK) channels. Examination of transgenic mice, each lacking one of the three SK channel genes expressed in the CNS, reveals that mice without the SK2 subunit completely lack the apamin-sensitive component of the ImAHP in CA1 neurons, whereas the IsAHP is not different in any of the SK transgenic mice. In each of the transgenic lines, the expression levels of the remaining SK genes are not changed. The results demonstrate that only SK2 channels are necessary for the ImAHP, and none of the SK channels underlie the IsAHP.

Indexed as

Long-Term PotentiationAnimalsApaminBlotting, WesternDose-Response Relationship, DrugEvoked PotentialsHippocampusIn Situ HybridizationMiceMice, KnockoutMice, TransgenicNeuronsPatch-Clamp TechniquesPolymerase Chain ReactionPotassium Channels, Calcium-ActivatedRNA, MessengerApaminPotassium Channels, Calcium-ActivatedRNA, Messenger

Identifiers

PMID15190101
PMCPMC2831645
OpenAlexW2170538656

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.