Evidence map›Paper›PMID 23575853›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

The neuroprotective drug riluzole acts via small conductance Ca2+-activated K+ channels to ameliorate defects in spinal muscular atrophy models.

Maria Dimitriadi, Min Jeong Kye, Geetika Kalloo, Jill M Yersak, Mustafa Sahin, Anne C Hart

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

34 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
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  6. Article
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  8. KJournal of neuroscience research · 2023
    Review
  9. Review
  10. KBiomedicines · 2023
    Review
  11. Article
  12. Subtype-selective positive modulation of KBritish journal of pharmacology · 2022
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Tetrodotoxin-Sensitive Neuronal-Type NaJournal of the American Heart Association · 2020
    Article
  20. Atomistic Insights of Calmodulin Gating of Complete Ion Channels.International journal of molecular sciences · 2020
    Review
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

6 authors at 3 institutions in 2 countries.

Maria DimitriadiDepartment of Neuroscience, Brown University, Providence, Rhode Island 02912, USA.
Min Jeong Kye
Geetika Kalloo
Jill M Yersak
Mustafa Sahin
Anne C Hart
Brown University · USBoston Children's Hospital · USHarvard University · US

Funding

SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI POMEROY, SCOTT LOREN · 1985 to 2015
$26.2M
Smn Regulation of Neuromuscular Morphogenesis in DrosophilaP01NS066888 · NINDS · HARVARD MEDICAL SCHOOL · PI ARTAVANIS-TSAKONAS, SPYRIDON · 2010 to 2014
$6.7M
NICHD NIH HHS P30 HD018655NICHD NIH HHS P30 HD18655NINDS NIH HHS NS066888NINDS NIH HHS P01 NS066888
6 · The paper itself

Abstract

Spinal muscular atrophy (SMA), a recessive neuromuscular disorder, is caused by diminished function of the Survival Motor Neuron (SMN) protein. To define the cellular processes pertinent to SMA, parallel genetic screens were undertaken in Drosophila and Caenorhabditis elegans SMA models to identify modifiers of the SMN loss of function phenotypes. One class of such genetic modifiers was the small conductance, Ca(2+)-activated K(+) (SK) channels. SK channels allow efflux of potassium ions when intracellular calcium increases and can be activated by the neuroprotective drug riluzole. The latter is the only drug with proven, albeit modest, efficacy in the treatment of amyotrophic lateral sclerosis. It is unclear if riluzole can extend life span or ameliorate symptoms in SMA patients as previous studies were limited and of insufficient power to draw any conclusions. The critical biochemical target of riluzole in motor neuron disease is not known, but the pharmacological targets of riluzole include SK channels. We examine here the impact of riluzole in two different SMA models. In vertebrate neurons, riluzole treatment restored axon outgrowth caused by diminished SMN. Additionally, riluzole ameliorated the neuromuscular defects in a C. elegans SMA model and SK channel function was required for this beneficial effect. We propose that riluzole improves motor neuron function by acting on SK channels and suggest that SK channels may be important therapeutic targets for SMA patients.

Indexed as

AnimalsAxonsCaenorhabditis elegansCells, CulturedDisease Models, AnimalGene Knockdown TechniquesHippocampusMuscular Atrophy, SpinalMutationNeuronsNeuroprotective AgentsRatsRats, Sprague-DawleyRiluzoleSmall-Conductance Calcium-Activated Potassium ChannelsSurvival of Motor Neuron 1 ProteinNeuroprotective AgentsRiluzoleSmall-Conductance Calcium-Activated Potassium ChannelsSurvival of Motor Neuron 1 Protein

Identifiers

PMID23575853
PMCPMC3652322
OpenAlexW2086311610

What OpenQuestion holds

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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.