Evidence map›Paper›PMID 20962215›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

A dominant mutation in a neuronal acetylcholine receptor subunit leads to motor neuron degeneration in Caenorhabditis elegans.

Belinda Barbagallo, Hilary A Prescott, Patrick Boyle, Jason Climer, Michael M Francis

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.7field-weighted citation impact, top 34% 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

25 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. A Novel and Functionally Diverse Class of Acetylcholine-Gated Ion Channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  3. Article
  4. The E3 ubiquitin ligase adaptorProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  5. Article
  6. Article
  7. The Role of CaCells · 2020
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. A Behavioral Survey of the Effects of Kavalactones onJournal of experimental neuroscience · 2017
    Article
  17. Article
  18. Expression of five acetylcholine receptor subunit genes in Brugia malayi adult worms.International journal for parasitology. Drugs and drug resistance · 2015
    Article
  19. Progressive degeneration of dopaminergic neurons through TRP channel-induced cell death.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    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

5 authors at 1 institution in 1 country.

Belinda BarbagalloDepartment of Neurobiology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA.
Hilary A Prescott
Patrick Boyle
Jason Climer
Michael M Francis
University of Massachusetts Chan Medical School · US

Funding

Molecular Analysis of Neural Circuit Excitation and InhibitionR01NS064263 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI FRANCIS, MICHAEL M · 2009 to 2025
$5.5M
Molecular analysis of neural circuit excitation and inhibitionR56NS064263 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI FRANCIS, MICHAEL M · 2015 to 2015
$419k
NINDS NIH HHS NS064263NINDS NIH HHS R01 NS064263NINDS NIH HHS R56 NS064263
6 · The paper itself

Abstract

Inappropriate or excessive activation of ionotropic receptors can have dramatic consequences for neuronal function and, in many instances, leads to cell death. In Caenorhabditis elegans, nicotinic acetylcholine receptor (nAChR) subunits are highly expressed in a neural circuit that controls movement. Here, we show that heteromeric nAChRs containing the acr-2 subunit are diffusely localized in the processes of excitatory motor neurons and act to modulate motor neuron activity. Excessive signaling through these receptors leads to cell-autonomous degeneration of cholinergic motor neurons and paralysis. C. elegans double mutants lacking calreticulin and calnexin-two genes previously implicated in the cellular events leading to necrotic-like cell death (Xu et al. 2001)-are resistant to nAChR-mediated toxicity and possess normal numbers of motor neuron cell bodies. Nonetheless, excess nAChR activation leads to progressive destabilization of the motor neuron processes and, ultimately, paralysis in these animals. Our results provide new evidence that chronic activation of ionotropic receptors can have devastating degenerative effects in neurons and reveal that ion channel-mediated toxicity may have distinct consequences in neuronal cell bodies and processes.

Indexed as

Amino Acid SubstitutionAnimalsBehavior, AnimalCaenorhabditis elegansCalnexinCalreticulinCell DeathGenes, ReporterHomeostasisIon ChannelsLocomotionMicroscopy, ConfocalMotor Neuron DiseaseNecrosisNerve DegenerationParalysisCalnexinCalreticulinIon ChannelsReceptors, Nicotinic

Identifiers

PMID20962215
PMCPMC2965043
OpenAlexW2076611356

What OpenQuestion holds

Textmetadata
LicenceTDM
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.