Evidence map›Paper›PMID 22539848›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012

Site-specific synapsin I phosphorylation participates in the expression of post-tetanic potentiation and its enhancement by BDNF.

Pierluigi Valente, Silvia Casagrande, Thierry Nieus, Anne M J Verstegen, Flavia Valtorta, Fabio Benfenati, Pietro Baldelli

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 59 citations in OpenAlex.

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  17. Impaired GABAOncotarget · 2017
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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

7 authors at 3 institutions in 1 country.

Pierluigi ValenteSection of Physiology, Department of Experimental Medicine, University of Genoa and National Institute of Neuroscience, 16132 Genova, Italy.
Silvia Casagrande
Thierry Nieus
Anne M J Verstegen
Flavia Valtorta
Fabio Benfenati
Pietro Baldelli
Italian Institute of Technology · ITUniversity of Genoa · ITVita-Salute San Raffaele University · IT

Funding

Telethon GGP09066Telethon GGP09134
6 · The paper itself

Abstract

A large amount of experimental evidence has highlighted the rapid changes in synaptic efficacy induced by high-frequency stimulation and BDNF at central excitatory synapses. We clarified the quantal mechanisms and the involvement of Synapsin I (SynI) phosphorylation in the expression of post-tetanic potentiation (PTP) and in its modulation by BDNF in mouse glutamatergic autapses. We found that PTP is associated with an elevation in the probability of release and a concomitant increase in the size of the readily releasable pool (RRP). The latter component was virtually absent in SynI knock-out (KO) neurons, which indeed displayed impaired PTP. PTP was fully rescued by the expression of wild-type SynI, but not of its dephosphomimetic mutants in the phosphorylation sites for cAMP-dependent protein kinase and Ca²⁺/calmodulin-dependent protein kinases I/II. BDNF potently enhanced PTP through a further increase in the RRP size, which was missing in SynI KO neurons. In these neurons, the BDNF-induced PTP enhancement was rescued by the expression of wild-type SynI, but not of its dephosphomimetic mutant at the mitogen-dependent protein kinase sites. The results indicate that the increase in RRP size necessary for the full expression of PTP, and its sensitivity to BDNF, involve phosphorylation of SynI at distinct sites, thus implicating SynI as an essential downstream effector for the expression of PTP and for its enhancement by BDNF.

Indexed as

6-Cyano-7-nitroquinoxaline-2,3-dioneAnalysis of VarianceAnimalsBiophysical PhenomenaBrain-Derived Neurotrophic FactorCalciumCarbazolesCells, CulturedElectric StimulationEmbryo, MammalianEnzyme InhibitorsExcitatory Amino Acid AntagonistsExcitatory Postsynaptic PotentialsGene Expression RegulationHippocampusIndole Alkaloids6-Cyano-7-nitroquinoxaline-2,3-dioneBrain-Derived Neurotrophic FactorCalciumCarbazolesEnzyme InhibitorsExcitatory Amino Acid AntagonistsIndole AlkaloidsMitogen-Activated Protein Kinase Kinasesstaurosporine aglyconeSynapsins

Identifiers

PMID22539848
PMCPMC6703602
OpenAlexW2044233480

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.