Evidence map›Paper›PMID 15483114›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004

Excessive expression of acetylcholinesterase impairs glutamatergic synaptogenesis in hippocampal neurons.

Haiheng Dong, Yun-Yan Xiang, Noa Farchi, William Ju, Yaojiong Wu, Liwen Chen, Yutian Wang, Binyamin Hochner, Burton Yang, Hermona Soreq and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 55 citations in OpenAlex.

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  12. Neurexin-1α regulates neurite growth of rat hippocampal neurons.International journal of physiology, pathophysiology and pharmacology · 2019
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  19. Increased transforming growth factor-β1 modulates glutamate receptor expression in the hippocampus.International journal of physiology, pathophysiology and pharmacology · 2011
    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

11 authors at 5 institutions in 3 countries.

Haiheng DongSunnybrook and Women's College Health Sciences Centre, University of Toronto, Toronto, Ontario, Canada M4N 3M5.
Yun-Yan Xiang
Noa Farchi
William Ju
Yaojiong Wu
Liwen Chen
Yutian Wang
Binyamin Hochner
Burton Yang
Hermona Soreq
Wei-Yang Lu
Health Sciences Centre · CAUniversity of Toronto · CAHebrew University of Jerusalem · ILInstitute of Neurobiology · BGSunnybrook Health Science Centre · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acetylcholinesterase (AChE) exerts noncatalytic activities on neural cell differentiation, adhesion, and neuritogenesis independently of its catalytic function. The noncatalytic functions of AChE have been attributed to its peripheral anionic site (PAS)-mediated protein-protein interactions. Structurally, AChE is highly homologous to the extracellular domain of neuroligin, a postsynaptic transmembrane molecule that interacts with presynaptic beta-neurexins, thus facilitating synaptic formation and maturation. Potential effects of AChE expression on synaptic transmission, however, remain unknown. Using electrophysiology, immunocytochemistry, and molecular biological approaches, this study investigated the role of AChE in the regulation of synaptic formation and functions. We found that AChE was highly expressed in cultured embryonic hippocampal neurons at early culture days, particularly in dendritic compartments including the growth cone. Subsequently, the expression level of AChE declined, whereas synaptic activity and synaptic proteins progressively increased. Chronic blockade of the PAS of AChE with specific inhibitors selectively impaired glutamatergic functions and excitatory synaptic structures independently of cholinergic activation, while inducing AChE overexpression. Moreover, the PAS blockade-induced glutamatergic impairments were associated with a depressed expression of beta-neurexins and an accumulation of other synaptic proteins, including neuroligins, and were mostly preventable by antisense suppression of AChE expression. Our findings demonstrate that interference with the nonenzymatic features of AChE alters AChE expression, which impairs excitatory synaptic structure and functions.

Indexed as

AcetylcholinesteraseAnimalsBinding SitesCells, CulturedCholinesterase InhibitorsEnzyme InhibitorsGlutamic AcidGrowth ConesHippocampusIn Situ HybridizationLigandsNerve Tissue ProteinsNeuronsPatch-Clamp TechniquesRatsRats, Sprague-DawleyAcetylcholinesteraseCholinesterase InhibitorsEnzyme InhibitorsGlutamic AcidLigandsNerve Tissue Proteinsneurexin IbetaReceptors, Glutamate

Identifiers

PMID15483114
PMCPMC6730061
OpenAlexW2145669366

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.