Evidence map›Paper›PMID 10212475›Full record

ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences1999

Synapsins as regulators of neurotransmitter release.

S Hilfiker, V A Pieribone, A J Czernik, H T Kao, G J Augustine, P Greengard

Open access · greenAbstract readReview
In one paragraph

Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 207 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
207citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 3% 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

207 citing papers in PubMed, 1 synthesis or guideline pooled it, 543 citations in OpenAlex.

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  19. Frequency of Spontaneous Neurotransmission at Individual Boutons Corresponds to the Size of the Readily Releasable Pool of Vesicles.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
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147 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 1 country.

S HilfikerLaboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, NY 10021, USA.
V A Pieribone
A J Czernik
H T Kao
G J Augustine
P Greengard
Rockefeller University · USDuke University · USJohn B. Pierce Laboratory · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One of the crucial issues in understanding neuronal transmission is to define the role(s) of the numerous proteins that are localized within presynaptic terminals and are thought to participate in the regulation of the synaptic vesicle life cycle. Synapsins are a multigene family of neuron-specific phosphoproteins and are the most abundant proteins on synaptic vesicles. Synapsins are able to interact in vitro with lipid and protein components of synaptic vesicles and with various cytoskeletal proteins, including actin. These and other studies have led to a model in which synapsins, by tethering synaptic vesicles to each other and to an actin-based cytoskeletal meshwork, maintain a reserve pool of vesicles in the vicinity of the active zone. Perturbation of synapsin function in a variety of preparations led to a selective disruption of this reserve pool and to an increase in synaptic depression, suggesting that the synapsin-dependent cluster of vesicles is required to sustain release of neurotransmitter in response to high levels of neuronal activity. In a recent study performed at the squid giant synapse, perturbation of synapsin function resulted in a selective disruption of the reserve pool of vesicles and in addition, led to an inhibition and slowing of the kinetics of neurotransmitter release, indicating a second role for synapsins downstream from vesicle docking. These data suggest that synapsins are involved in two distinct reactions which are crucial for exocytosis in presynaptic nerve terminals. This review describes our current understanding of the molecular mechanisms by which synapsins modulate synaptic transmission, while the increasingly well-documented role of the synapsins in synapse formation and stabilization lies beyond the scope of this review.

Indexed as

AnimalsGene ExpressionHumansIn Vitro TechniquesLipidsMicroscopy, ElectronModels, NeurologicalNerve Tissue ProteinsNeuronal PlasticityNeurotransmitter AgentsPhosphorylationSynapsesSynapsinsLipidsNerve Tissue ProteinsNeurotransmitter AgentsSynapsins

Identifiers

PMID10212475
PMCPMC1692497
OpenAlexW2022740810

What Socratic 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 Socratic graph.