Evidence map›Paper›PMID 10517801›Full record

ArticleThe Journal of physiology1999

Modulation by K+ channels of action potential-evoked intracellular Ca2+ concentration rises in rat cerebellar basket cell axons.

Y P Tan, I Llano

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

36 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. The potassium channel subunit KProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  6. Article
  7. Alteration of Neuronal Excitability and Short-Term Synaptic Plasticity in the Prefrontal Cortex of a Mouse Model of Mental Illness.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Cellular mechanisms and behavioral consequences of Kv1.2 regulation in the rat cerebellum.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  13. Article
  14. A new Kv1.2 channelopathy underlying cerebellar ataxia.The Journal of biological chemistry · 2010
    Article
  15. Article
  16. Voltage-gated potassium channels in human immunodeficiency virus type-1 (HIV-1)-associated neurocognitive disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2009
    Review
  17. Article
  18. Recurrent axon collaterals underlie facilitating synapses between cerebellar Purkinje cells.Proceedings of the National Academy of Sciences of the United States of America · 2007
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Y P TanArbeitsgruppe Zellulare Neurobiologie, Max-Planck-Institut fur biophysikalische Chemie, Am Fassberg, D-37070 Gottingen, Germany.
I Llano
Max Planck Institute for Biophysical Chemistry · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. Action potential-evoked [Ca2+]i rises in basket cell axons of rat cerebellar slices were studied using two-photon laser scanning microscopy and whole-cell recording, to identify the K+ channels controlling the shape of the axonal action potential. 2. Whole-cell recordings of Purkinje cell IPSCs were used to screen K+ channel subtypes which could contribute to axonal repolarization. alpha-Dendrotoxin, 4-aminopyridine, charybdotoxin and tetraethylammonium chloride increased IPSC rate and/or amplitude, whereas iberiotoxin and apamin failed to affect the IPSCs. 3. The effects of those K+ channel blockers that enhanced transmitter release on the [Ca2+]i rises elicited in basket cell axons by action potentials fell into three groups: 4-aminopyridine strongly increased action potential-evoked [Ca2+]i; tetraethylammonium and charybdotoxin were ineffective alone but augmented the effects of 4-aminopyridine; alpha-dendrotoxin had no effect. 4. We conclude that cerebellar basket cells contain at least three pharmacologically distinct K+ channels, which regulate transmitter release through different mechanisms. 4-Aminopyridine-sensitive, alpha-dendrotoxin-insensitive K+ channels are mainly responsible for repolarization in basket cell presynaptic terminals. K+ channels blocked by charybdotoxin and tetraethylammonium have a minor role in repolarization. alpha-Dendrotoxin-sensitive channels are not involved in shaping the axonal action potential waveform. The two last types of channels must therefore exert control of synaptic activity through a pathway unrelated to axonal action potential broadening.

Indexed as

4-AminopyridineAction PotentialsAnimalsAxonsCalciumCerebellumElapid VenomsElectrophysiologyExcitatory Postsynaptic PotentialsIn Vitro TechniquesNeurotoxinsPatch-Clamp TechniquesPotassium Channel BlockersPotassium ChannelsPresynaptic TerminalsPurkinje Cells4-AminopyridineCalciumdendrotoxinElapid VenomsNeurotoxinsPotassium Channel BlockersPotassium Channels

Identifiers

PMID10517801
PMCPMC2269558
OpenAlexW2138274361

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.