Evidence map›Paper›PMID 20016093›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009

Synchronous and asynchronous transmitter release at nicotinic synapses are differentially regulated by postsynaptic PSD-95 proteins.

Robert A Neff, William G Conroy, Jeffrey D Schoellerman, Darwin K Berg

Open access · bronzeAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. A novel mechanism for nicotinic potentiation of glutamatergic synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  4. Review
  5. Review
  6. Article
  7. PMCA2 via PSD-95 controls calcium signaling by α7-containing nicotinic acetylcholine receptors on aspiny interneurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  8. Article
  9. Article
  10. Lateral mobility of nicotinic acetylcholine receptors on neurons is determined by receptor composition, local domain, and cell type.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    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

4 authors at 1 institution in 1 country.

Robert A NeffNeurobiology Section, Division of Biological Sciences, University of California, San Diego, La Jolla, California 92093-0357, USA.
William G Conroy
Jeffrey D Schoellerman
Darwin K Berg
University of California, San Diego · US

Funding

Signal Transduction at Neuronal Nicotinic SynapsesR01NS012601 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BERG, DARWIN K · 1985 to 2016
$5.3M
Nicotinic Control of Non-Nicotinic Synapses in the HippocampusR01NS035469 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BERG, DARWIN K · 1996 to 2013
$4.8M
NINDS NIH HHS NS012601NINDS NIH HHS NS035469NINDS NIH HHS R01 NS012601NINDS NIH HHS R01 NS035469
6 · The paper itself

Abstract

The rate and timing of information transfer at neuronal synapses are critical for determining synaptic efficacy and higher network function. Both synchronous and asynchronous neurotransmitter release shape the pattern of synaptic influences on a neuron. The PSD-95 family of postsynaptic scaffolding proteins, in addition to organizing postsynaptic components at glutamate synapses, acts transcellularly to regulate synchronous glutamate release. Here we show that PSD-95 family members at nicotinic synapses on chick ciliary ganglion neurons in culture execute multiple functions to enhance transmission. Together, endogenous PSD-95 and SAP102 in the postsynaptic cell appear to regulate transcellularly the synchronous release of transmitter from presynaptic terminals onto the neuron while stabilizing postsynaptic nicotinic receptor clusters under the release sites. Endogenous SAP97, in contrast, has no effect on receptor clusters but acts transcellularly from the postsynaptic cell through N-cadherin to enhance asynchronous release. These separate and parallel regulatory pathways allow postsynaptic scaffold proteins to dictate the pattern of cholinergic input a neuron receives; they also require balancing of PSD-95 protein levels to avoid disruptive competition that can occur through common binding domains.

Indexed as

AnimalsAvian ProteinsCell LineCells, CulturedChick EmbryoDisks Large Homolog 4 ProteinExcitatory Postsynaptic PotentialsGanglia, ParasympatheticGene Knockdown TechniquesHumansIntracellular Signaling Peptides and ProteinsMembrane ProteinsNeurotransmitter AgentsNuclear ProteinsReceptors, NicotinicRNA InterferenceAvian ProteinsDisks Large Homolog 4 ProteinDLG3 protein, humanDLG4 protein, humanIntracellular Signaling Peptides and ProteinsMembrane ProteinsNeurotransmitter AgentsNuclear ProteinsReceptors, NicotinicTranscription Factors

Identifiers

PMID20016093
PMCPMC2844112
OpenAlexW2070920901

What OpenQuestion holds

Textmetadata
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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.