Evidence map›Paper›PMID 23073716›Full record

ArticleNeuromolecular medicine2013

Hypoxia markers are expressed in interneurons exposed to recurrent seizures.

Fabio Gualtieri, Carla Marinelli, Daniela Longo, Matteo Pugnaghi, Paolo F Nichelli, Stefano Meletti, Giuseppe Biagini

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In one paragraph

Article in Neuromolecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Circumscribing Laser Cuts Attenuate Seizure Propagation in a Mouse Model of Focal Epilepsy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  7. Staining Hypoxic Areas of Frozen and FFPE Tissue Sections with Hypoxyprobe™.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. The Neuroprotective Effect ofInternational journal of molecular sciences · 2019
    Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. 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

7 authors at 2 institutions in 2 countries.

Fabio GualtieriDipartimento di Scienze Biomediche, Metaboliche e Neuroscienze, Laboratorio di Epilettologia Sperimentale, Università di Modena e Reggio Emilia, Via Campi 287, 41125, Modena, Italy.
Carla Marinelli
Daniela Longo
Matteo Pugnaghi
Paolo F Nichelli
Stefano Meletti
Giuseppe Biagini
University of Modena and Reggio Emilia · ITNational Operating Committee on Standards for Athletic Equipment · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An early but transient decrease in oxygen availability occurs during experimentally induced seizures. Using pimonidazole, which probes hypoxic insults, we found that by increasing the duration of pilocarpine-induced status epilepticus (SE) from 30 to 120 min, counts of pimonidazole-immunoreactive neurons also increased (P < 0.01, 120 vs 60 and 30 min). All the animals exposed to SE were immunopositive to pimonidazole, but a different scenario emerged during epileptogenesis when a decrease in pimonidazole-immunostained cells occurred from 7 to 14 days, so that only 1 out of 4 rats presented with pimonidazole-immunopositive cells. Pimonidazole-immunoreactive cells robustly reappeared at 21 days post-SE induction when all animals (7 out of 7) had developed spontaneous recurrent seizures. Specific neuronal markers revealed that immunopositivity to pimonidazole was present in cells identified by neuropeptide Y (NPY) or somatostatin antibodies. At variance, neurons immunopositive to parvalbumin or cholecystokinin were not immunopositive to pimonidazole. Pimonidazole-immunopositive neurons expressed remarkable immunoreactivity to hypoxia-inducible factor 1α (HIF-1α). Interestingly, surgical samples obtained from pharmacoresistant patients showed neurons co-labeled by HIF-1α and NPY antibodies. These interneurons, along with parvalbumin-positive interneurons that were negative to HIF-1α, showed immunopositivity to markers of cell damage, such as high-mobility group box 1 in the cytoplasm and cleaved caspase-3 in the nucleus. These findings suggest that interneurons are continuously endangered in rodent and human epileptogenic tissue. The presence of hypoxia and cell damage markers in NPY interneurons of rats and patients presenting with recurrent seizures indicates a mechanism of selective vulnerability in a specific neuronal subpopulation.

Indexed as

Cell HypoxiaAnimalsAnticonvulsantsBiomarkersCerebral CortexConvulsantsDiazepamDisease ProgressionDrug ResistanceEpilepsyHMGB1 ProteinHumansHypoxia-Inducible Factor 1, alpha SubunitInterneuronsMaleNerve Tissue ProteinsAnticonvulsantsBiomarkersConvulsantsDiazepamHIF1A protein, humanHMGB1 ProteinHypoxia-Inducible Factor 1, alpha SubunitNerve Tissue ProteinsNeuropeptide YNitroimidazolesParvalbuminsPilocarpinepimonidazole

Identifiers

PMID23073716
OpenAlexW2091436938

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.