Evidence map›Paper›PMID 19052202›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008

Fgf-2 overexpression increases excitability and seizure susceptibility but decreases seizure-induced cell loss.

Silvia Zucchini, Andrea Buzzi, Mario Barbieri, Donata Rodi, Beatrice Paradiso, Anna Binaschi, J Douglas Coffin, Andrea Marzola, Pierangelo Cifelli, Ottorino Belluzzi and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

21 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. FGF family in health and disease.Molecular biomedicine · 2026
    Review
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  7. Astrocyte-derived extracellular vesicles: Neuroreparative properties and role in the pathogenesis of neurodegenerative disorders.Journal of controlled release : official journal of the Controlled Release Society · 2020
    Review
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  13. FGF Signaling Is Necessary for Neurogenesis in Young Mice and Sufficient to Reverse Its Decline in Old Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
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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

11 authors at 2 institutions in 2 countries.

Silvia ZucchiniSection of Pharmacology, Department of Clinical Experimental Medicine, Section of Pathology, National Institute of Neuroscience and Neuroscience Center, University of Ferrara, 44100 Ferrara, Italy.
Andrea Buzzi
Mario Barbieri
Donata Rodi
Beatrice Paradiso
Anna Binaschi
J Douglas Coffin
Andrea Marzola
Pierangelo Cifelli
Ottorino Belluzzi
Michele Simonato
University of Ferrara · ITUniversity of Montana · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibroblast growth factor 2 (FGF-2) has multiple, pleiotropic effects on the nervous system that include neurogenesis, neuroprotection and neuroplasticity. Thus, alteration in FGF-2 expression patterns may have a profound impact in brain function, both in normal physiology and in pathology. Here, we used FGF-2 transgenic mice (TgFGF2) to study the effects of endogenous FGF-2 overexpression on susceptibility to seizures and to the pathological consequences of seizures. TgFGF2 mice display increased FGF-2 expression in hippocampal pyramidal neurons and dentate granule cells. Increased density of glutamatergic synaptic vesicles was observed in the hippocampus of TgFGF2 mice, and electrophysiological data (input/output curves and patch-clamp recordings in CA1) confirmed an increase in excitatory inputs in CA1, suggesting the presence of a latent hyperexcitability. Indeed, TgFGF2 mice displayed increased susceptibility to kainate-induced seizures compared with wild-type (WT) littermates, in that latency to generalized seizure onset was reduced, whereas behavioral seizure scores and lethality were increased. Finally, WT and TgFGF2 mice with similar seizure scores were used for examining seizure-induced cellular consequences. Neurogenesis and mossy fiber sprouting were not significantly different between the two groups. In contrast, cell damage (assessed with Fluoro-Jade B, silver impregnation and anti-caspase 3 immunohistochemistry) was significantly lower in TgFGF2 mice, especially in the areas of overexpression (CA1 and CA3), indicating reduction of seizure-induced necrosis and apoptosis. These data suggest that FGF-2 may be implicated in seizure susceptibility and in seizure-induced plasticity, exerting different, and apparently contrasting effects: favoring ictogenesis but reducing seizure-induced cell death.

Indexed as

AnimalsCell DeathConvulsantsDisease Models, AnimalEpilepsyFemaleFibroblast Growth Factor 2Genetic Predisposition to DiseaseGlutamic AcidGrowth ConesHippocampusHumansMaleMembrane PotentialsMiceMice, TransgenicConvulsantsFibroblast Growth Factor 2Glutamic Acid

Identifiers

PMID19052202
PMCPMC3844742
OpenAlexW2041778633

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.