Evidence map›Paper›PMID 30952836›Full record

ArticleCell death & disease2019

Dynamic interplay between H-current and M-current controls motoneuron hyperexcitability in amyotrophic lateral sclerosis.

Yossi Buskila, Orsolya Kékesi, Alba Bellot-Saez, Winston Seah, Tracey Berg, Michael Trpceski, Justin J Yerbury, Lezanne Ooi

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 41 citations in OpenAlex.

  1. ALS-FTD-linked CCNFJournal of neuroinflammation · 2026
    Article
  2. Roles of funny HCN.Comparative biochemistry and physiology. Toxicology & pharmacology : CBP · 2025
    Review
  3. Review
  4. Tau-mediated synaptic dysfunction is coupled with HCN channelopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  5. Review
  6. Alzheimer's disease induced neurons bearingFrontiers in cellular neuroscience · 2024
    Article
  7. Article
  8. Astrocytic modulation of neuronal signalling.Frontiers in network physiology · 2023
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Neuromodulation of Glial Function During Neurodegeneration.Frontiers in cellular neuroscience · 2020
    Article
  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

8 authors at 3 institutions in 1 country.

Yossi BuskilaBiomedical Engineering and Neuroscience research group, The MARCS Institute, Western Sydney University, Penrith, NSW, 2751, Australia. Y.buskila@westernsydney.edu.au.
Orsolya KékesiBiomedical Engineering and Neuroscience research group, The MARCS Institute, Western Sydney University, Penrith, NSW, 2751, Australia.
Alba Bellot-SaezBiomedical Engineering and Neuroscience research group, The MARCS Institute, Western Sydney University, Penrith, NSW, 2751, Australia.
Winston SeahBiomedical Engineering and Neuroscience research group, The MARCS Institute, Western Sydney University, Penrith, NSW, 2751, Australia.
Tracey BergSchool of Chemistry and Molecular Bioscience, University of Wollongong, Northfields Avenue, Wollongong, NSW, 2522, Australia.
Michael TrpceskiSchool of Chemistry and Molecular Bioscience, University of Wollongong, Northfields Avenue, Wollongong, NSW, 2522, Australia.
Justin J YerburySchool of Chemistry and Molecular Bioscience, University of Wollongong, Northfields Avenue, Wollongong, NSW, 2522, Australia.
Lezanne OoiSchool of Chemistry and Molecular Bioscience, University of Wollongong, Northfields Avenue, Wollongong, NSW, 2522, Australia. lezanne@uow.edu.au.
University of Wollongong · AUCamden and Campbelltown Hospitals · AUIllawarra Health and Medical Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a type of motor neuron disease (MND) in which humans lose motor functions due to progressive loss of motoneurons in the cortex, brainstem, and spinal cord. In patients and in animal models of MND it has been observed that there is a change in the properties of motoneurons, termed neuronal hyperexcitability, which is an exaggerated response of the neurons to a stimulus. Previous studies suggested neuronal excitability is one of the leading causes for neuronal loss, however the factors that instigate excitability in neurons over the course of disease onset and progression are not well understood, as these studies have looked mainly at embryonic or early postnatal stages (pre-symptomatic). As hyperexcitability is not a static phenomenon, the aim of this study was to assess the overall excitability of upper motoneurons during disease progression, specifically focusing on their oscillatory behavior and capabilities to fire repetitively. Our results suggest that increases in the intrinsic excitability of motoneurons are a global phenomenon of aging, however the cellular mechanisms that underlie this hyperexcitability are distinct in SOD1

Indexed as

AgingCortical ExcitabilityAmyotrophic Lateral SclerosisAnimalsDisease Models, AnimalDisease ProgressionFemaleHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsKCNQ Potassium ChannelsMaleMembrane PotentialsMiceMice, TransgenicMotor NeuronsSuperoxide Dismutase-1Hyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsKCNQ Potassium ChannelsSuperoxide Dismutase-1

Identifiers

PMID30952836
PMCPMC6450866
OpenAlexW2930959407

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.