Evidence map›Paper›PMID 18057210›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007

Lack of synapsin I reduces the readily releasable pool of synaptic vesicles at central inhibitory synapses.

Pietro Baldelli, Anna Fassio, Flavia Valtorta, Fabio Benfenati

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
3.0field-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

85 citing papers in PubMed, 172 citations in OpenAlex.

  1. Article
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  7. Review
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  12. Synapse-Specific Defects in Synaptic Transmission in the Cerebellum of W246G Mutant ELOVL4 Rats-a Model of Human SCA34.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  13. The SphK1/S1P Axis Regulates Synaptic Vesicle Endocytosis via TRPC5 Channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  14. Article
  15. Synapsin III gene silencing redeems alpha-synuclein transgenic mice from Parkinson's disease-like phenotype.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  16. Review
  17. Review
  18. Alterations of presynaptic proteins in autism spectrum disorder.Frontiers in molecular neuroscience · 2022
    Review
  19. Article
  20. Function of Drosophila Synaptotagmins in membrane trafficking at synapses.Cellular and molecular life sciences : CMLS · 2021
    Review

25 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

4 authors at 3 institutions in 1 country.

Pietro BaldelliDepartment of Neuroscience and Brain Technologies, The Italian Institute of Technology, 16163 Genova, Italy. pietro.baldelli@unige.it
Anna Fassio
Flavia Valtorta
Fabio Benfenati
University of Genoa · ITItalian Institute of Technology · ITVita-Salute San Raffaele University · IT

Funding

Telethon GGP05134
6 · The paper itself

Abstract

Synapsins (Syns) are synaptic vesicle (SV) phosphoproteins that play a role in neurotransmitter release and synaptic plasticity by acting at multiple steps of exocytosis. Mutation of SYN genes results in an epileptic phenotype in mouse and man suggesting a role of Syns in the control of network excitability. We have studied the effects of the genetic ablation of the SYN1 gene on inhibitory synaptic transmission in primary hippocampal neurons. Inhibitory neurons lacking SynI showed reduced amplitude of IPSCs evoked by isolated action potentials. The impairment in inhibitory transmission was caused by a decrease in the size of the SV readily releasable pool, rather than by changes in release probability or quantal size. The reduction of the readily releasable pool was caused by a decrease in the number of SVs released by single synaptic boutons in response to the action potential, in the absence of variations in the number of synaptic contacts between couples of monosynaptically connected neurons. The deletion of SYN1 did not affect paired-pulse depression or post-tetanic potentiation, but was associated with a moderate increase of synaptic depression evoked by trains of action potentials, which became apparent at high stimulation frequencies and was accompanied by a slow down of recovery from depression. The decreased size of the SV readily releasable pool, coupled with a decreased SV recycling rate and refilling by the SV reserve pool, may contribute to the epileptic phenotype of SynI knock-out mice.

Indexed as

AnimalsCells, CulturedHippocampusInhibitory Postsynaptic PotentialsMiceMice, KnockoutNeural InhibitionSynapsesSynapsinsSynaptic VesiclesSynapsins

Identifiers

PMID18057210
PMCPMC6673103
OpenAlexW2060227133

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.