Evidence map›Paper›PMID 9736663›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998

Critical role of axonal A-type K+ channels and axonal geometry in the gating of action potential propagation along CA3 pyramidal cell axons: a simulation study.

I L Kopysova, D Debanne

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. The metabolic role of vagal afferent innervation.Nature reviews. Gastroenterology & hepatology · 2018
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Inside the brain of a neuron.EMBO reports · 2006
    Review
  13. Article
  14. Determinants of action potential propagation in cerebellar Purkinje cell axons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005
    Article
  15. Article
  16. Axonal propagation: does the spike stop here?The Journal of physiology · 2003
    Article
  17. Action potentials reliably invade axonal arbors of rat neocortical neurons.Proceedings of the National Academy of Sciences of the United States of America · 2000
    Article
  18. Release-independent short-term synaptic depression in cultured hippocampal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000
    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

2 authors at 2 institutions in 2 countries.

I L KopysovaUnité de Neurocybernétique Cellulaire, UPR 9041 Centre National de la Recherche Scientifique, 13009 Marseille, France.
D Debanne
Centre National de la Recherche Scientifique · FRHumboldt-Universität zu Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A model of CA3 pyramidal cell axons was used to study a new mode of gating of action potential (AP) propagation along the axon that depends on the activation of A-type K+ current (Debanne et al., 1997). The axonal membrane contained voltage-dependent Na+ channels, K+ channels, and A-type K+ channels. The density of axonal A-channels was first determined so that (1) at the resting membrane potential an AP elicited by a somatic depolarization was propagated into all axon collaterals and (2) propagation failures occurred when a brief somatic hyperpolarization preceded the AP induction. Both conditions were fulfilled only when A-channels were distributed in clusters but not when they were homogeneously distributed along the axon. Failure occurs in the proximal part of the axon. Conduction failure could be determined by a single cluster of A-channels, local decrease of axon diameter, or axonal elongation. We estimated the amplitude and temporal parameters of the hyperpolarization required for induction of a conduction block. Transient and small somatic hyperpolarizations, such as simulated GABAA inhibitory postsynaptic potentials, were able to block the AP propagation. It was shown that AP induction had to occur with a short delay (<30 msec) after the hyperpolarization. We discuss the possible conditions in which such local variations of the axon geometry and A-channel density may occur and the incidence of AP propagation failures on hippocampal network properties.

Indexed as

Computer SimulationModels, NeurologicalAction PotentialsAnimalsAxonsExcitatory Postsynaptic PotentialsHippocampusIon Channel GatingKineticsNeural ConductionNeural InhibitionNeuronal PlasticityPotassium ChannelsPyramidal CellsReceptors, GABA-ASodium ChannelsPotassium ChannelsReceptors, GABA-ASodium Channels

Identifiers

PMID9736663
PMCPMC6793228
OpenAlexW1512813107

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.