Evidence map›Paper›PMID 11826094›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002

Specific gap junctions enhance the neuronal vulnerability to brain traumatic injury.

Marina V Frantseva, Larisa Kokarovtseva, Christian G Naus, Peter L Carlen, Derrick MacFabe, Jose L Perez Velazquez

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

87 citing papers in PubMed, 213 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Role of astrocytes connexins - pannexins in acute brain injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Cell Death and Recovery in Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020
    Review
  14. Review
  15. Connexin Signaling Is Involved in the Reactivation of a Latent Stem Cell Niche after Spinal Cord Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

27 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

6 authors at 4 institutions in 2 countries.

Marina V FrantsevaThe Hospital for Sick Children, Toronto, Ontario, M5G 1X8, Canada.
Larisa Kokarovtseva
Christian G Naus
Peter L Carlen
Derrick MacFabe
Jose L Perez Velazquez
Hospital for Sick Children · CAInstitute of Cell Biology and Neurobiology · ITToronto Western Hospital · CAWestern University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic brain injury results in neuronal loss and associated neurological deficits. Although most research on the factors leading to trauma-induced damage focuses on synaptic or ionic mechanisms, the possible role of direct intercellular communication via gap junctions has remained unexplored. Gap junctions connect directly the cytoplasms of coupled cells; hence, they offer a way to propagate stress signals from cell to cell. We investigated the contribution of gap junctional communication (GJC) to cell death using an in vitro trauma model. The impact injury, induced by a weight dropped on the distal CA1 area of organotypic hippocampal slices, results in glutamate-dependent cell loss. The gap junctional blockers carbenoxolone and octanol decreased significantly post-traumatic cell death, measured by propidium iodide staining over a 72 hr period after the impact. Dye coupling in the pyramidal layers was enhanced immediately after the injury and decreased over the following 24 hr. To determine whether specific connexins were involved in the spread of trauma-induced cell death, we used organotypic slices from connexin43 (Cx43) knock-out mice, as well as acute knock-outs by incubation with antisense oligodeoxynucleotides. Simultaneous knockdown of two neuronal connexins resulted in significant neuroprotection. Slices from the null-mutant Cx43 mice, as well as the acute Cx43 knockdown, also showed decreased cell death after the impact. The gap junctional blockers alleviated the trauma-induced impairment of synaptic function as measured by electrophysiological field potential recordings. These results indicate that GJC enhances the cellular vulnerability to traumatic injury. Hence, specific gap junctions could be a novel target to reduce injury and secondary damage to the brain and maximize recovery from trauma.

Indexed as

Cell CommunicationAnimalsAnimals, NewbornBrain InjuriesCarbenoxoloneCell CountCell DeathConnexin 26Connexin 43ConnexinsDisease SusceptibilityFluoresceinsGap Junction beta-1 ProteinGap JunctionsHippocampusIn Vitro TechniquesCarbenoxoloneConnexin 26Connexin 43ConnexinsdiacetylfluoresceinFluoresceinsGap Junction beta-1 ProteinOctanolsOligonucleotides, Antisense

Identifiers

PMID11826094
PMCPMC6758478
OpenAlexW1648606954

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.