Evidence map›Paper›PMID 9223334›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1997

Acetylcholinesterase-transgenic mice display embryonic modulations in spinal cord choline acetyltransferase and neurexin Ibeta gene expression followed by late-onset neuromotor deterioration.

C Andres, R Beeri, A Friedman, E Lev-Lehman, S Henis, R Timberg, M Shani, H Soreq

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

19 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
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  6. Neurexin-neuroligin signaling in synapse development.Current opinion in neurobiology · 2007
    Review
  7. Review
  8. Article
  9. Excessive expression of acetylcholinesterase impairs glutamatergic synaptogenesis in hippocampal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Excess "read-through" acetylcholinesterase attenuates but the "synaptic" variant intensifies neurodeterioration correlates.Proceedings of the National Academy of Sciences of the United States of America · 2000
    Article
  15. Article
  16. Functional redundancy of acetylcholinesterase and neuroligin in mammalian neuritogenesis.Proceedings of the National Academy of Sciences of the United States of America · 1998
    Article
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  18. Article
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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

8 authors at 2 institutions in 1 country.

C AndresDepartment of Biological Chemistry, The Hebrew University of Jerusalem, 91904 Israel.
R Beeri
A Friedman
E Lev-Lehman
S Henis
R Timberg
M Shani
H Soreq
Hebrew University of Jerusalem · ILAgricultural Research Organization · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To explore the possibility that overproduction of neuronal acetylcholinesterase (AChE) confers changes in both cholinergic and morphogenic intercellular interactions, we studied developmental responses to neuronal AChE overexpression in motoneurons and neuromuscular junctions of AChE-transgenic mice. Perikarya of spinal cord motoneurons were consistently enlarged from embryonic through adult stages in AChE-transgenic mice. Atypical motoneuron development was accompanied by premature enhancement in the embryonic spinal cord expression of choline acetyltransferase mRNA, encoding the acetylcholine-synthesizing enzyme choline acetyltransferase. In contrast, the mRNA encoding for neurexin-Ibeta, the heterophilic ligand of the AChE-homologous neuronal cell surface protein neuroligin, was drastically lower in embryonic transgenic spinal cord than in controls. Postnatal cessation of these dual transcriptional responses was followed by late-onset deterioration in neuromotor performance that was associated with gross aberrations in neuromuscular ultrastructure and with pronounced amyotrophy. These findings demonstrate embryonic feedback mechanisms to neuronal AChE overexpression that are attributable to both cholinergic and cell-cell interaction pathways, suggesting that embryonic neurexin Ibeta expression is concerted in vivo with AChE levels and indicating that postnatal changes in neuronal AChE-associated proteins may be involved in late-onset neuromotor pathologies.

Indexed as

AcetylcholinesteraseAnimalsCholine O-AcetyltransferaseElectromyographyGene Expression Regulation, DevelopmentalGene Expression Regulation, EnzymologicHumansMiceMice, TransgenicMotor NeuronsNerve Tissue ProteinsNeuromuscular JunctionRNA, MessengerSpinal CordAcetylcholinesteraseCholine O-AcetyltransferaseNerve Tissue Proteinsneurexin IbetaRNA, Messenger

Identifiers

PMID9223334
PMCPMC21576
OpenAlexW2048975846

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.