Evidence map›Paper›PMID 23252894›Full record

ReviewAnnals of the New York Academy of Sciences2012

Active zones of mammalian neuromuscular junctions: formation, density, and aging.

Hiroshi Nishimune

Open access · greenAbstract readReview
In one paragraph

Review in Annals of the New York Academy of Sciences, 2012. 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
0.8field-weighted citation impact, top 28% 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, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Macrophage Depletion Ameliorates Peripheral Neuropathy in Aging Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  9. Review
  10. Article
  11. Review
  12. Neuromuscular Junction Dismantling in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2017
    Review
  13. The role of laminins in the organization and function of neuromuscular junctions.Matrix biology : journal of the International Society for Matrix Biology · 2017
    Review
  14. Article
  15. Synaptic Deficits at Neuromuscular Junctions in Two Mouse Models of Charcot-Marie-Tooth Type 2d.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  16. Article
  17. Review
  18. Article
  19. Review
  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

1 author at 1 institution in 1 country.

Hiroshi NishimuneDepartment of Anatomy and Cell Biology, University of Kansas Medical School, Kansas City, 66160, USA. hnishimune@kumc.edu
University of Kansas · US

Funding

Research Design and Analysis Core (RDAC)P30HD002528 · NICHD · UNIVERSITY OF KANSAS LAWRENCE · PI FOWLER, STEPHEN CLETIUS · 1985 to 2015
$22.1M
U KANSAS COBRE ADMINISTRATIVE COREP20RR024214 · NCRR · UNIVERSITY OF KANSAS MEDICAL CENTER · PI KRIEG, ADAM J · 2007 to 2011
$10.8M
Active zone loss cause dying back neuropathy in amyotrophic lateral sclerosisR01NS078214 · NINDS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI NISHIMUNE, HIROSHI · 2012 to 2016
$1.6M
NCRR NIH HHS P20 RR024214NCRR NIH HHS RR024214NICHD NIH HHS HD002528NICHD NIH HHS P30 HD002528NINDS NIH HHS R01 NS078214
6 · The paper itself

Abstract

Presynaptic active zones are synaptic vesicle release sites that play essential roles in the function and pathology of mammalian neuromuscular junctions (NMJs). The molecular mechanisms of active zone organization use presynaptic voltage-dependent calcium channels (VDCCs) in NMJs as scaffolding proteins. VDCCs interact extracellularly with the muscle-derived synapse organizer, laminin β2 and interact intracellularly with active zone-specific proteins, such as Bassoon, CAST/Erc2/ELKS2alpha, ELKS, Piccolo, and RIMs. These molecular mechanisms are supported by studies in P/Q- and N-type VDCCs double-knockout mice, and they are consistent with the pathological conditions of Lambert-Eaton myasthenic syndrome and Pierson syndrome, which are caused by autoantibodies against VDCCs or by a laminin β2 mutation. During normal postnatal maturation, NMJs maintain the density of active zones, while NMJs triple their size. However, active zones become impaired during aging. Propitiously, muscle exercise ameliorates the active zone impairment in aged NMJs, which suggests the potential for therapeutic strategies.

Indexed as

Abnormalities, MultipleAgingAnimalsAutoantibodiesCalcium ChannelsEye AbnormalitiesHumansLambert-Eaton Myasthenic SyndromeMyasthenic Syndromes, CongenitalNephrotic SyndromeNerve Tissue ProteinsNeuromuscular JunctionPresynaptic TerminalsPupil DisordersAutoantibodiesCalcium ChannelsNerve Tissue Proteins

Identifiers

PMID23252894
PMCPMC3531881
OpenAlexW2115456845

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.