Evidence map›Paper›PMID 18354015›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008

Evidence for muscle-dependent neuromuscular synaptic site determination in mammals.

Vita M Vock, Olga N Ponomareva, Mendell Rimer

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Motor function recovery: deciphering a regenerative niche at the neuromuscular synapse.Biological reviews of the Cambridge Philosophical Society · 2021
    Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Stem cell-derived tissue-engineered constructs for hemilaryngeal reconstruction.The Annals of otology, rhinology, and laryngology · 2014
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Rescuing Z+ agrin splicing in Nova null mice restores synapse formation and unmasks a physiologic defect in motor neuron firing.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Article
  17. Muscle-wide secretion of a miniaturized form of neural agrin rescues focal neuromuscular innervation in agrin mutant mice.Proceedings of the National Academy of Sciences of the United States of America · 2008
    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 1 institution in 1 country.

Vita M VockSection of Neurobiology, University of Texas at Austin, Austin, Texas 78712, USA.
Olga N Ponomareva
Mendell Rimer
The University of Texas at Austin · US

Funding

Neuregulin-2 and the formation of neuromuscular synapsesR01GM065797 · NIGMS · UNIVERSITY OF TEXAS AUSTIN · PI RIMER, MENDELL · 2002 to 2006
$1.0M
NIGMS NIH HHS GM065797NIGMS NIH HHS R01 GM065797
6 · The paper itself

Abstract

Recent evidence challenges the prevalent view that neural factors induce the formation of a de novo postsynaptic apparatus during development of the vertebrate neuromuscular junction. The latest experiments suggest an alternative model in which the muscle fiber induces a nascent postsynaptic apparatus and sets the location of the future synapse. On axonal contact, these sites, laid out in a prepattern in the central area of developing muscle fibers, mature into synapses by the combined action of neural factors such as agrin and ACh. We sought to test in mammals these two models of neuromuscular synaptogenesis. Previously, we showed that continuous prenatal muscle expression of constitutively active ErbB2 (CAErbB2) led to synaptic loss, exuberant axonal sprouting, and lethality at birth. Here, we transiently induced CAErbB2 during midgestation and examined synapse restoration after inducer withdrawal. Centrally enriched ACh receptor (AChR) transcription and clustering were abolished after transient CAErbB2 induction. After inducer withdrawal, synapses were restored but were distributed widely over the entire diaphragm muscle. Under the nerve-dependent model, this distribution is explained by the wide pattern of axonal sprouting triggered by CAErbB2. Yet, in the absence of the nerve, introduced in our animals by mating to Hb9(+/-) mice, a very similar, wide distribution of aneural AChR clusters resulted. Thus, transient expression of CAErbB2 in skeletal muscles leads to reprogramming of the endogenous muscle AChR prepattern. This, and not the nerve, seems primarily responsible for the widely distributed pattern of synapses in our experimental animals.

Indexed as

AnimalsAnimals, NewbornBungarotoxinsDiaphragmDoxycyclineEmbryo, MammalianErb-b2 Receptor Tyrosine KinasesFemaleGene Expression Regulation, DevelopmentalGreen Fluorescent ProteinsHomeodomain ProteinsLuciferasesMaleMiceMice, TransgenicMicroscopy, ConfocalBungarotoxinsDoxycyclineErb-b2 Receptor Tyrosine KinasesGreen Fluorescent ProteinsHb9 protein, mouseHomeodomain ProteinsLuciferasesMuSK protein, ratReceptor Protein-Tyrosine KinasesReceptors, CholinergicTranscription Factors

Identifiers

PMID18354015
PMCPMC6670698
OpenAlexW2072026493

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.