Evidence map›Paper›PMID 22615428›Full record

ArticleThe Journal of physiology2012

A-type K+ channels encoded by Kv4.2, Kv4.3 and Kv1.4 differentially regulate intrinsic excitability of cortical pyramidal neurons.

Yarimar Carrasquillo, Andreas Burkhalter, Jeanne M Nerbonne

Abstract read
In one paragraph

Article in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
–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

57 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Design of Ultrapotent Genetically Encoded Inhibitors of Kv4.2 for Gating Neural Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
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  6. Review
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  15. Pharmacology of A-Type KHandbook of experimental pharmacology · 2021
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Altered gating of KeLife · 2019
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

Yarimar CarrasquilloDepartment of Developmental Biology, Washington University School of Medicine, 660 South Euclid Avenue, Campus Box 8103, St Louis, MO 63110, USA.
Andreas Burkhalter
Jeanne M Nerbonne

Funding

CARDIOVASCULAR SYSTEM--FUNCTION/REGULATION/PHARMACOLOGYT32HL007275 · NHLBI · WASHINGTON UNIVERSITY · PI NERBONNE, JEANNE M. · 1985 to 2013
$6.0M
CORTICAL CIRCUITRY FOR TOP-DOWN SELECTION OF VISUAL INPUTSR01EY020523 · NEI · WASHINGTON UNIVERSITY · PI BURKHALTER, ANDREAS HANS · 2010 to 2013
$1.5M
Molecular Dissection of Neuronal K+ Channel FunctionR01NS041417 · NINDS · WASHINGTON UNIVERSITY · PI NERBONNE, JEANNE M. · 2002 to 2005
$1.0M
KV CHANNEL FUNCTIONING IN MACROMOLECULAR COMPLEXESR21NS065295 · NINDS · WASHINGTON UNIVERSITY · PI NERBONNE, JEANNE M. · 2009 to 2010
$416k
Novel role for SCN1b as a modulator of Kv4.2 channels and neuronal excitabilityF32NS065581 · NINDS · WASHINGTON UNIVERSITY · PI CARRASQUILLO-GARCIA, YARIMAR · 2009 to 2010
$106k
NEI NIH HHS R01 EY020523NHLBI NIH HHS T32 HL007275NHLBI NIH HHS T32-HL007275NINDS NIH HHS F32 NS065581NINDS NIH HHS F32-NS065581NINDS NIH HHS R01 NS041417NINDS NIH HHS R01-NS041417NINDS NIH HHS R01-NS065295NINDS NIH HHS R21 NS065295
6 · The paper itself

Abstract

Rapidly activating and rapidly inactivating voltage-gated A-type K+ currents, IA, are key determinants of neuronal excitability and several studies suggest a critical role for the Kv4.2 pore-forming α subunit in the generation of IA channels in hippocampal and cortical pyramidal neurons. The experiments here demonstrate that Kv4.2, Kv4.3 and Kv1.4 all contribute to the generation of IA channels in mature cortical pyramidal (CP) neurons and that Kv4.2-, Kv4.3- and Kv1.4-encoded IA channels play distinct roles in regulating the intrinsic excitability and the firing properties of mature CP neurons. In vivo loss of Kv4.2, for example, alters the input resistances, current thresholds for action potential generation and action potential repolarization of mature CP neurons. Elimination of Kv4.3 also prolongs action potential duration, whereas the input resistances and the current thresholds for action potential generation in Kv4.3−/− and WT CP neurons are indistinguishable. In addition, although increased repetitive firing was observed in both Kv4.2−/− and Kv4.3−/− CP neurons, the increases in Kv4.2−/− CP neurons were observed in response to small, but not large, amplitude depolarizing current injections, whereas firing rates were higher in Kv4.3−/− CP neurons only with large amplitude current injections. In vivo loss of Kv1.4, in contrast, had minimal effects on the intrinsic excitability and the firing properties of mature CP neurons. Comparison of the effects of pharmacological blockade of Kv4-encoded currents in Kv1.4−/− and WT CP neurons, however, revealed that Kv1.4-encoded IA channels do contribute to controlling resting membrane potentials, the regulation of current thresholds for action potential generation and repetitive firing rates in mature CP neurons.

Indexed as

AnimalsGene Expression RegulationKv1.4 Potassium ChannelMembrane PotentialsMiceNeuronsPyramidal TractsShal Potassium ChannelsKcna4 protein, mouseKv1.4 Potassium ChannelShal Potassium Channels

Identifiers

PMID22615428
PMCPMC3476638

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.