Evidence map›Paper›PMID 18684905›Full record

ArticleJournal of neurophysiology2008

Function of neuromuscular synapses in the zebrafish choline-acetyltransferase mutant bajan.

Meng Wang, Hua Wen, Paul Brehm

Open access · greenAbstract read
In one paragraph

Article in Journal of neurophysiology, 2008. 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
1.1field-weighted citation impact, top 24% 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, 33 citations in OpenAlex.

  1. Article
  2. Context-dependent hyperactivity inFrontiers in molecular neuroscience · 2024
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Fatigue in Rapsyn-Deficient Zebrafish Reflects Defective Transmitter Release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  12. Article
  13. Defects of the Glycinergic Synapse in Zebrafish.Frontiers in molecular neuroscience · 2016
    Review
  14. Article
  15. Review
  16. Mapping a sensory-motor network onto a structural and functional ground plan in the hindbrain.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  17. Article
  18. Distinct retinal deficits in a zebrafish pyruvate dehydrogenase-deficient mutant.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    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

3 authors at 2 institutions in 1 country.

Meng WangDepartment of Neurobiology and Behavior, Stony Brook University, Stony Brook, NY, USA.
Hua Wen
Paul Brehm
Vollum Institute · USStony Brook University · US

Funding

Regulation of Acetylcholine Receptors on MuscleR37NS018205 · NINDS · STATE UNIVERSITY NEW YORK STONY BROOK · PI BREHM, PAUL · 2005 to 2011
$2.4M
REGULATION OF ACETYLCHOLINE RECEPTORS ON MUSCLER01NS018205 · NINDS · TUFTS UNIVERSITY BOSTON · PI BREHM, PAUL · 1985 to 2004
$1.8M
In Vivo Analysis of Synaptic Function in ZebrafishF32NS052078 · NINDS · STATE UNIVERSITY NEW YORK STONY BROOK · PI WEN, HUA · 2006 to 2007
$103k
NINDS NIH HHS NS-052078NINDS NIH HHS NS-18205
6 · The paper itself

Abstract

We have identified a zebrafish mutant line, bajan, in which compromised motility and fatigue result from a point mutation in the gene coding choline acetyltransferase (ChAT), the enzyme responsible for acetylcholine (ACh) synthesis. Although the mutation predicts loss of ChAT function, bajan inexplicably retains low levels of neuromuscular transmission. We exploited this residual activity and determined the consequences for synaptic function. The attenuated synaptic responses were a direct consequence of a decrease in both resting mean quantal size and quantal content. To replicate behavioral fatigue in swimming, motorneurons were stimulated at high frequencies. A prominent reduction in quantal content, reflecting vesicle depletion, was coincident with a small additional reduction in quantal size. In humans, defective ChAT leads to episodic apnea, a form of congenital myasthenic syndrome characterized by use-dependent fatigue. In contrast to bajan, however, afflicted individuals exhibit a normal resting quantal size and quantal content. The fatigue in humans results from a pronounced long-lasting drop in quantal size with little or no change in quantal content. These differences have important implications for interpreting fatigue as well as on understanding the impact of ACh availability on vesicle filling and recycling.

Indexed as

AnimalsCholine O-AcetyltransferaseDNA, ComplementaryElectrophysiologyImmunohistochemistryIn Vitro TechniquesLarvaMicroscopy, ConfocalMotor EndplateMutationNeuromuscular JunctionNeurotransmitter AgentsOligonucleotidesPatch-Clamp TechniquesReceptors, PresynapticStereotyped BehaviorCholine O-AcetyltransferaseDNA, ComplementaryNeurotransmitter AgentsOligonucleotidesReceptors, Presynaptic

Identifiers

PMID18684905
PMCPMC2576202
OpenAlexW2031129628

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.