Evidence map›Paper›PMID 25556795›Full record

ArticleThe Journal of physiology2015

KV 10.1 opposes activity-dependent increase in Ca²⁺ influx into the presynaptic terminal of the parallel fibre-Purkinje cell synapse.

Lena Sünke Mortensen, Hartmut Schmidt, Zohreh Farsi, Alonso Barrantes-Freer, María E Rubio, Roser Ufartes, Jens Eilers, Takeshi Sakaba, Walter Stühmer, Luis A Pardo

Open access · hybridAbstract read
In one paragraph

Article in The Journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. The Kv10.1 Channel: A Promising Target in Cancer.International journal of molecular sciences · 2022
    Review
  10. Article
  11. Review
  12. Article
  13. The EAG Voltage-Dependent KFrontiers in pharmacology · 2020
    Review
  14. Potassium Channel Gain of Function in Epilepsy: An Unresolved Paradox.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2018
    Article
  15. Regulation of Eag by CaJournal of neurophysiology · 2018
    Article
  16. Ether-à-go-go KThe Journal of physiology · 2018
    Review
  17. A new mechanism of voltage-dependent gating exposed by KThe Journal of general physiology · 2017
    Article
  18. Review
  19. Article
  20. 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

10 authors at 3 institutions in 2 countries.

Lena Sünke MortensenMax-Planck-Institute of Experimental Medicine, 37075, Göttingen, Germany; International Max Planck Research School Neurosciences, 37077, Göttingen, Germany.
Hartmut Schmidt
Zohreh Farsi
Alonso Barrantes-Freer
María E Rubio
Roser Ufartes
Jens Eilers
Takeshi Sakaba
Walter Stühmer
Luis A Pardo
Max Planck Institute of Experimental Medicine · DELudwig Cancer Research · BEMax Planck Institute for Biophysical Chemistry · DE

Funding

Mechanisms of hypersensitivity to sound-induced cochlear damageR01DC013048 · NIDCD · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Maria-Eulalia Rubio-Valero · 2013 to 2026
$6.8M
NIDCD NIH HHS 1R01DC013048-01
6 · The paper itself

Abstract

key pointsVoltage-gated KV 10.1 potassium channels are widely expressed in the mammalian brain but their function remains poorly understood. We report that KV 10.1 is enriched in the presynaptic terminals and does not take part in somatic action potentials. In parallel fibre synapses in the cerebellar cortex, we find that KV 10.1 regulates Ca(2+) influx and neurotransmitter release during repetitive high-frequency activity. Our results describe the physiological role of mammalian KV 10.1 for the first time and help understand the fine-tuning of synaptic transmission. The voltage-gated potassium channel KV 10.1 (Eag1) is widely expressed in the mammalian brain, but its physiological function is not yet understood. Previous studies revealed highest expression levels in hippocampus and cerebellum and suggested a synaptic localization of the channel. The distinct activation kinetics of KV 10.1 indicate a role during repetitive activity of the cell. Here, we confirm the synaptic localization of KV 10.1 both biochemically and functionally and that the channel is sufficiently fast at physiological temperature to take part in repolarization of the action potential (AP). We studied the role of the channel in cerebellar physiology using patch clamp and two-photon Ca(2+) imaging in KV 10.1-deficient and wild-type mice. The excitability and action potential waveform recorded at granule cell somata was unchanged, while Ca(2+) influx into axonal boutons was enhanced in mutants in response to stimulation with three APs, but not after a single AP. Furthermore, mutants exhibited a frequency-dependent increase in facilitation at the parallel fibre-Purkinje cell synapse at high firing rates. We propose that KV 10.1 acts as a modulator of local AP shape specifically during high-frequency burst firing when other potassium channels suffer cumulative inactivation.

Indexed as

Action PotentialsAnimalsCalciumCerebellumEther-A-Go-Go Potassium ChannelsExcitatory Postsynaptic PotentialsHEK293 CellsHumansMice, KnockoutPotassium Channels, Voltage-GatedPurkinje CellsRats, Sprague-DawleySynapsesCalciumEther-A-Go-Go Potassium ChannelsKcng3 protein, mouseKCNH1 protein, humanPotassium Channels, Voltage-Gated

Identifiers

PMID25556795
PMCPMC4293062
OpenAlexW2153878385

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.