Evidence map›Paper›PMID 22326946›Full record

ReviewBiochimica et biophysica acta2013

Gap junction communication in myelinating glia.

Anna Nualart-Marti, Carles Solsona, R Douglas Fields

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
4.3field-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

59 citing papers in PubMed, 113 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Neuroglial Pathophysiology of Leukodystrophies.Advances in neurobiology · 2025
    Review
  6. Oligodendrocytes: Myelination, Plasticity, and Axonal Support.Cold Spring Harbor perspectives in biology · 2024
    Review
  7. Review
  8. Review
  9. Innexin-Mediated Adhesion between Glia Is Required for Axon Ensheathment in the Peripheral Nervous System.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. How Does the Immune System Enter the Brain?Frontiers in immunology · 2022
    Review
  15. Review
  16. Article
  17. Review
  18. Energy Metabolism in the Inner Retina in Health and Glaucoma.International journal of molecular sciences · 2021
    Review
  19. Review
  20. 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

3 authors at 2 institutions in 2 countries.

Anna Nualart-MartiDepartment of Pathology and Experimental Therapeutics, University of Barcelona, Barcelona, Spain. annanualart@ub.edu
Carles Solsona
R Douglas Fields
National Institutes of Health · USBellvitge University Hospital · ES

Funding

Nervous System Development and PlasticityZIAHD000713 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI FIELDS, RICHARD DOUGLAS · 2009 to 2023
$17.7M
Intramural NIH HHS ZIA HD000713
6 · The paper itself

Abstract

Gap junction communication is crucial for myelination and axonal survival in both the peripheral nervous system (PNS) and central nervous system (CNS). This review examines the different types of gap junctions in myelinating glia of the PNS and CNS (Schwann cells and oligodendrocytes respectively), including their functions and involvement in neurological disorders. Gap junctions mediate intercellular communication among Schwann cells in the PNS, and among oligodendrocytes and between oligodendrocytes and astrocytes in the CNS. Reflexive gap junctions mediating transfer between different regions of the same cell promote communication between cellular compartments of myelinating glia that are separated by layers of compact myelin. Gap junctions in myelinating glia regulate physiological processes such as cell growth, proliferation, calcium signaling, and participate in extracellular signaling via release of neurotransmitters from hemijunctions. In the CNS, gap junctions form a glial network between oligodendrocytes and astrocytes. This transcellular communication is hypothesized to maintain homeostasis by facilitating restoration of membrane potential after axonal activity via electrical coupling and the re-distribution of potassium ions released from axons. The generation of transgenic mice for different subsets of connexins has revealed the contribution of different connexins in gap junction formation and illuminated new subcellular mechanisms underlying demyelination and cognitive defects. Alterations in metabolic coupling have been reported in animal models of X-linked Charcot-Marie-Tooth disease (CMTX) and Pelizaeus-Merzbarcher-like disease (PMLD), which are caused by mutations in the genes encoding for connexin 32 and connexin 47 respectively. Future research identifying the expression and regulation of gap junctions in myelinating glia is likely to provide a better understanding of myelinating glia in nervous system function, plasticity, and disease. This article is part of a Special Issue entitled: The Communicating junctions, roles and dysfunctions.

Indexed as

Adenosine TriphosphateAnimalsCell CommunicationCell Membrane PermeabilityConnexinsDemyelinating DiseasesGap JunctionsHumansMutationMyelin SheathNeurogliaAdenosine TriphosphateConnexins

Identifiers

PMID22326946
PMCPMC4474145
OpenAlexW2003945891

What OpenQuestion holds

Textmetadata
LicenceTDM
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.