Evidence map›Paper›PMID 25438677›Full record

ArticleCNS neuroscience & therapeutics2015

In Rasmussen encephalitis, hemichannels associated with microglial activation are linked to cortical pyramidal neuron coupling: a possible mechanism for cellular hyperexcitability.

Carlos Cepeda, Julia W Chang, Geoffrey C Owens, My N Huynh, Jane Y Chen, Conny Tran, Harry V Vinters, Michael S Levine, Gary W Mathern

Open access · bronzeAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2015. 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
1.5field-weighted citation impact, top 21% 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, 33 citations in OpenAlex.

  1. Review
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  8. Review
  9. Insights into Potential Targets for Therapeutic Intervention in Epilepsy.International journal of molecular sciences · 2020
    Review
  10. Pannexin-1 Deficiency Decreases Epileptic Activity in Mice.International journal of molecular sciences · 2020
    Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Diseases associated with leaky hemichannels.Frontiers in cellular neuroscience · 2015
    Review
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

9 authors at 3 institutions in 1 country.

Carlos CepedaIntellectual and Developmental Disabilities Research Center, Brain Research Institute, Los Angeles, CA, USA.
Julia W Chang
Geoffrey C Owens
My N Huynh
Jane Y Chen
Conny Tran
Harry V Vinters
Michael S Levine
Gary W Mathern
Department of Behavioral Health and Intellectual Disability Services · USUniversity of California, Los Angeles · USMattel Children's Hospital · US

Funding

UCLA MSD ProgramR25GM055052 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BARBER, PAUL HENRY, HASSON, TAMA W. · 1996 to 2021
$9.2M
Project 3. Genetic Models of Human Structural Brain Defects in ZebrafishP01HD070494 · NICHD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLEESON, JOSEPH G · 2011 to 2016
$6.7M
PATHOPHYSIOLOGY OF DEVELOPING DYSPLASTIC HUMAN CORTEXR01NS038992 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CEPEDA, CARLOS T, MATHERN, GARY W. · 1999 to 2013
$3.3M
Molecular characterization of HemimegalencephalyR01NS083823 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLEESON, JOSEPH G, MATHERN, GARY W. · 2013 to 2017
$3.1M
NICHD NIH HHS P01 HD070494NINDS NIH HHS NS 38992NINDS NIH HHS R01 NS038992NINDS NIH HHS R01 NS083823
6 · The paper itself

Abstract

aimsRasmussen encephalitis (RE) is a rare but devastating condition, mainly in children, characterized by sustained brain inflammation, atrophy of one cerebral hemisphere, epilepsy, and progressive cognitive deterioration. The etiology of RE-induced seizures associated with the inflammatory process remains unknown.

methodsCortical tissue samples from children undergoing surgical resections for the treatment of RE (n = 16) and non-RE (n = 12) were compared using electrophysiological, morphological, and immunohistochemical techniques to examine neuronal properties and the relationship with microglial activation using the specific microglia/macrophage calcium-binding protein, IBA1 in conjunction with connexins and pannexin expression.

resultsCompared with non-RE cases, pyramidal neurons from RE cases displayed increased cell capacitance and reduced input resistance. However, neuronal somatic areas were not increased in size. Instead, intracellular injection of biocytin led to increased dye coupling between neurons from RE cases. By Western blot, expression of IBA1 and pannexin was increased while connexin 32 was decreased in RE cases compared with non-RE cases. IBA1 immunostaining overlapped with pannexin and connexin 36 in RE cases.

conclusionsIn RE, these results support the notion that a possible mechanism for cellular hyperexcitability may be related to increased intercellular coupling from pannexin linked to increased microglial activation. Such findings suggest that a possible antiseizure treatment for RE may involve the use of gap junction blockers.

Indexed as

4-AminopyridineAdolescentBiophysicsCalcium-Binding ProteinsCerebral CortexChildCohort StudiesConnexinsDNA-Binding ProteinsElectric StimulationEncephalitisExcitatory Postsynaptic PotentialsFemaleHumansIn Vitro TechniquesLysine4-AminopyridineAIF1 protein, humanbiocytinCalcium-Binding ProteinsConnexinsDNA-Binding ProteinsLysineMefloquineMicrofilament ProteinsPotassium Channel BlockersGap junctionsHyperexcitabilityPannexinRasmussen encephalitis

Identifiers

PMID25438677
PMCPMC4303544
OpenAlexW2021477438

What OpenQuestion holds

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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.