Evidence map›Paper›PMID 12223564›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002

Extrasynaptic alpha 7-nicotinic acetylcholine receptor expression in developing neurons is regulated by inputs, targets, and activity.

Craig L Brumwell, James L Johnson, Michele H Jacob

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

15 citing papers in PubMed, 34 citations in OpenAlex.

  1. Temporal regulation of nicotinic acetylcholine receptor subunits supports central cholinergic synapse development inProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Implications of activity-dependent neurotransmitter-receptor matching.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2008
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Functional mapping and Ca2+ regulation of nicotinic acetylcholine receptor channels in rat hippocampal CA1 neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003
    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.

Craig L BrumwellDepartment of Neuroscience, Tufts University, Sackler School of Biomedical Sciences, Boston, Massachusetts 02111, USA.
James L Johnson
Michele H Jacob
Tufts University · US

Funding

Regulation- Medulloblastoma Growth by alpha-v integrinsK08CA092056 · NCI · CHILDREN'S RESEARCH INSTITUTE · PI MACDONALD, TOBEY J · 2002 to 2006
$636k
NCI NIH HHS K08 CA092056PHS HHS 21725
6 · The paper itself

Abstract

Alpha7-nicotinic acetylcholine receptors (nAChRs) are widely expressed in the vertebrate nervous system. alpha7-nAChR functions include postsynaptic transmission, modulating neurotransmitter release, reinforcing nicotine addiction, and a role in neurological disorders, such as schizophrenia and Alzheimer's disease. In chick parasympathetic ciliary ganglion (CG) neurons, alpha7-nAChRs are excluded from the synapse and localize perisynaptically. Despite their extrasynaptic distribution, the highly Ca2+-permeable alpha7-nAChRs have important synapse-related Ca2+-dependent signaling functions in the CG. We show here that the synaptic partners regulate alpha7-nAChR expression during synapse formation in embryonic CG neurons in situ. The absence of inputs and target tissues cause reductions in alpha7-nAChR mRNA and protein levels that primarily resemble those seen for synaptic alpha3-nAChRs. However, there is a difference in their regulation. alpha7-nAChR levels are downregulated by reduced activity, whereas alpha3-nAChR levels are not. We propose that the activity-dependent regulation of extrasynaptic alpha7-nAChR levels may be an important mechanism for postsynaptic CG neurons to detect changes in presynaptic activity levels and respond with Ca2+-dependent plasticity changes in gene expression.

Indexed as

alpha7 Nicotinic Acetylcholine ReceptorAnimalsCalciumCell CountChick EmbryoDenervationGanglia, ParasympatheticGanglia, SympatheticGene Expression Regulation, DevelopmentalNeuronal PlasticityNeuronsProtein SubunitsReceptors, NicotinicRNA, MessengerSensory DeprivationSynapsesalpha7 Nicotinic Acetylcholine ReceptorCalciumProtein SubunitsReceptors, NicotinicRNA, Messenger

Identifiers

PMID12223564
PMCPMC6758097
OpenAlexW2134896896

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.