Evidence map›Paper›PMID 26733679›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Sympathetic innervation controls homeostasis of neuromuscular junctions in health and disease.

Muzamil Majid Khan, Danilo Lustrino, Willian A Silveira, Franziska Wild, Tatjana Straka, Yasmin Issop, Emily O'Connor, Dan Cox, Markus Reischl, Till Marquardt and 10 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
8.6field-weighted citation impact, top 2% 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

91 citing papers in PubMed, 158 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Increased Homer Activity and NMJ Localization in the Vestibular LesionInternational journal of molecular sciences · 2024
    Article
  19. Review
  20. Article

31 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 10 institutions in 5 countries.

Muzamil Majid KhanInterdisciplinary Center for Neurosciences, Universität Heidelberg, 69120 Heidelberg, Germany; Institute of Molecular and Cell Biology, Hochschule Mannheim, 68163 Mannheim, Germany; Institute of Toxicology and Genetics, Karlsruhe Institute of Technology, 76344 Eggenstein-Leopoldshafen, Germany;
Danilo LustrinoDepartment of Physiology, Faculdade de Medicina de Ribeirão Preto, University of São Paulo, 14049-900 Ribeirão Preto, Brazil; Department of Biochemistry and Immunology, Faculdade de Medicina de Ribeirão Preto, University of São Paulo, 14049-900 Ribeirão Preto, Brazil;
Willian A SilveiraDepartment of Physiology, Faculdade de Medicina de Ribeirão Preto, University of São Paulo, 14049-900 Ribeirão Preto, Brazil; Department of Biochemistry and Immunology, Faculdade de Medicina de Ribeirão Preto, University of São Paulo, 14049-900 Ribeirão Preto, Brazil;
Franziska WildInterdisciplinary Center for Neurosciences, Universität Heidelberg, 69120 Heidelberg, Germany; Institute of Molecular and Cell Biology, Hochschule Mannheim, 68163 Mannheim, Germany; Institute of Toxicology and Genetics, Karlsruhe Institute of Technology, 76344 Eggenstein-Leopoldshafen, Germany;
Tatjana StrakaInterdisciplinary Center for Neurosciences, Universität Heidelberg, 69120 Heidelberg, Germany; Institute of Molecular and Cell Biology, Hochschule Mannheim, 68163 Mannheim, Germany; Institute of Toxicology and Genetics, Karlsruhe Institute of Technology, 76344 Eggenstein-Leopoldshafen, Germany;
Yasmin IssopThe John Walton Muscular Dystrophy Research Centre, Medical Research Council Centre for Neuromuscular Diseases, Newcastle University, Newcastle upon Tyne NE1 3BZ, United Kingdom;
Emily O'ConnorThe John Walton Muscular Dystrophy Research Centre, Medical Research Council Centre for Neuromuscular Diseases, Newcastle University, Newcastle upon Tyne NE1 3BZ, United Kingdom;
Dan CoxThe John Walton Muscular Dystrophy Research Centre, Medical Research Council Centre for Neuromuscular Diseases, Newcastle University, Newcastle upon Tyne NE1 3BZ, United Kingdom;
Markus ReischlInstitute of Applied Informatics, Karlsruhe Institute of Technology, 76344 Eggenstein-Leopoldshafen, Germany;
Till MarquardtDevelopmental Neurobiology Laboratory, European Neuroscience Institute, 37077 Göttingen, Germany;
Dittmar LabeitDepartment of Integrative Pathophysiology, Universität Heidelberg, 68167 Mannheim, Germany;
Siegfried LabeitDepartment of Integrative Pathophysiology, Universität Heidelberg, 68167 Mannheim, Germany;
Evelyne BenoitCommissariat a l'energie atomique, Institut de Biologie et Technologies de Saclay (iBiTec-S), Service d'Ingénierie Moléculaire des Protéines (SIMOPRO), 91191 Gif-sur-Yvette Cedex, France; Institut des Neurosciences Paris-Saclay, UMR 9197, CNRS/Université Paris-Sud, 91190 Gif-sur-Yvette Cedex, France;
Jordi MolgóCommissariat a l'energie atomique, Institut de Biologie et Technologies de Saclay (iBiTec-S), Service d'Ingénierie Moléculaire des Protéines (SIMOPRO), 91191 Gif-sur-Yvette Cedex, France; Institut des Neurosciences Paris-Saclay, UMR 9197, CNRS/Université Paris-Sud, 91190 Gif-sur-Yvette Cedex, France;
Hanns LochmüllerThe John Walton Muscular Dystrophy Research Centre, Medical Research Council Centre for Neuromuscular Diseases, Newcastle University, Newcastle upon Tyne NE1 3BZ, United Kingdom;
Veit WitzemannMax Planck Institute for Medical Research, 69120 Heidelberg, Germany;
Isis C KettelhutDepartment of Physiology, Faculdade de Medicina de Ribeirão Preto, University of São Paulo, 14049-900 Ribeirão Preto, Brazil; Department of Biochemistry and Immunology, Faculdade de Medicina de Ribeirão Preto, University of São Paulo, 14049-900 Ribeirão Preto, Brazil;
Luiz C C NavegantesDepartment of Physiology, Faculdade de Medicina de Ribeirão Preto, University of São Paulo, 14049-900 Ribeirão Preto, Brazil; Department of Biochemistry and Immunology, Faculdade de Medicina de Ribeirão Preto, University of São Paulo, 14049-900 Ribeirão Preto, Brazil;
Tullio PozzanDepartment of Biomedical Sciences, University of Padua, 35121 Padua, Italy; Institute of Neuroscience, Padua Section, National Research Council, 35121 Padua, Italy tullio.pozzan@unipd.it r.rudolf@hs-mannheim.de.
Rüdiger RudolfInterdisciplinary Center for Neurosciences, Universität Heidelberg, 69120 Heidelberg, Germany; Institute of Molecular and Cell Biology, Hochschule Mannheim, 68163 Mannheim, Germany; Institute of Toxicology and Genetics, Karlsruhe Institute of Technology, 76344 Eggenstein-Leopoldshafen, Germany; tullio.pozzan@unipd.it r.rudolf@hs-mannheim.de.
Karlsruhe Institute of Technology · DEUniversidade de São Paulo · BRHeidelberg University · DEInstitut des Neurosciences Paris-Saclay · FRMedical Research Council · GBNewcastle University · GBEuropean Neuroscience Institute Göttingen · DEMannheim University of Applied Sciences · DEMax Planck Institute for Medical Research · DEUniversity of Padua · IT

Funding

Medical Research Council 98482Medical Research Council G1002274Medical Research Council MR/K000608/1
6 · The paper itself

Abstract

The distribution and function of sympathetic innervation in skeletal muscle have largely remained elusive. Here we demonstrate that sympathetic neurons make close contact with neuromuscular junctions and form a network in skeletal muscle that may functionally couple different targets including blood vessels, motor neurons, and muscle fibers. Direct stimulation of sympathetic neurons led to activation of muscle postsynaptic β2-adrenoreceptor (ADRB2), cAMP production, and import of the transcriptional coactivator peroxisome proliferator-activated receptor γ-coactivator 1α (PPARGC1A) into myonuclei. Electrophysiological and morphological deficits of neuromuscular junctions upon sympathectomy and in myasthenic mice were rescued by sympathicomimetic treatment. In conclusion, this study identifies the neuromuscular junction as a target of the sympathetic nervous system and shows that sympathetic input is crucial for synapse maintenance and function.

Indexed as

HealthHomeostasisActive Transport, Cell NucleusAnimalsBiosensing TechniquesCell NucleusCyclic AMPFemaleMaleMice, Inbred C57BLModels, BiologicalMuscle, SkeletalNervous System DiseasesNeuromuscular JunctionNeuronsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaCyclic AMPPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseTranscription Factorsbeta-agonistscAMPmyasthenianeuromuscular junctionsympathetic neurons

Identifiers

PMID26733679
PMCPMC4725522
OpenAlexW2223176310

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.