Evidence map›Paper›PMID 24587109›Full record

ArticlePloS one2014

Progressive brain damage, synaptic reorganization and NMDA activation in a model of epileptogenic cortical dysplasia.

Francesca Colciaghi, Adele Finardi, Paola Nobili, Denise Locatelli, Giada Spigolon, Giorgio Stefano Battaglia

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. CNS autoimmune response in the MAM/pilocarpine rat model of epileptogenic cortical malformation.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

6 authors at 1 institution in 1 country.

Francesca ColciaghiMolecular Neuroanatomy and Pathogenesis Unit, IRCCS Neurological Institute "C. Besta", Milano, Italy.
Adele FinardiMolecular Neuroanatomy and Pathogenesis Unit, IRCCS Neurological Institute "C. Besta", Milano, Italy.
Paola NobiliMolecular Neuroanatomy and Pathogenesis Unit, IRCCS Neurological Institute "C. Besta", Milano, Italy.
Denise LocatelliMolecular Neuroanatomy and Pathogenesis Unit, IRCCS Neurological Institute "C. Besta", Milano, Italy.
Giada SpigolonNeuroscience Institute Cavalieri Ottolenghi (NICO), University of Torino, Orbassano (Torino), Italy.
Giorgio Stefano BattagliaMolecular Neuroanatomy and Pathogenesis Unit, IRCCS Neurological Institute "C. Besta", Milano, Italy.
Neuroscience Institute · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Whether severe epilepsy could be a progressive disorder remains as yet unresolved. We previously demonstrated in a rat model of acquired focal cortical dysplasia, the methylazoxymethanol/pilocarpine - MAM/pilocarpine - rats, that the occurrence of status epilepticus (SE) and subsequent seizures fostered a pathologic process capable of modifying the morphology of cortical pyramidal neurons and NMDA receptor expression/localization. We have here extended our analysis by evaluating neocortical and hippocampal changes in MAM/pilocarpine rats at different epilepsy stages, from few days after onset up to six months of chronic epilepsy. Our findings indicate that the process triggered by SE and subsequent seizures in the malformed brain i) is steadily progressive, deeply altering neocortical and hippocampal morphology, with atrophy of neocortex and CA regions and progressive increase of granule cell layer dispersion; ii) changes dramatically the fine morphology of neurons in neocortex and hippocampus, by increasing cell size and decreasing both dendrite arborization and spine density; iii) induces reorganization of glutamatergic and GABAergic networks in both neocortex and hippocampus, favoring excitatory vs inhibitory input; iv) activates NMDA regulatory subunits. Taken together, our data indicate that, at least in experimental models of brain malformations, severe seizure activity, i.e., SE plus recurrent seizures, may lead to a widespread, steadily progressive architectural, neuronal and synaptic reorganization in the brain. They also suggest the mechanistic relevance of glutamate/NMDA hyper-activation in the seizure-related brain pathologic plasticity.

Indexed as

AnimalsAtrophyCerebral CortexDisease Models, AnimalEpilepsies, PartialFemaleHippocampusMalformations of Cortical DevelopmentNeocortexN-MethylaspartatePregnancyPyramidal CellsRatsReceptors, N-Methyl-D-AspartateSynapsesN-MethylaspartateReceptors, N-Methyl-D-Aspartate

Identifiers

PMID24587109
PMCPMC3937400
OpenAlexW2078747521

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.