Brain connexins in demyelinating diseases: Therapeutic potential of glial targets

Abstract Several demyelinating syndromes have been linked to mutations in glial gap junction proteins, the connexins. Although mutations in connexins of the myelinating cells, Schwann cells and oligodendrocytes, were initially described, recent data have shown that astrocytes also play a major role...

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Bibliographic Details
Published in:Brain research 2012-12, Vol.1487, p.61-68
Main Authors: Cotrina, Maria Luisa, Nedergaard, Maiken
Format: Article
Language:English
Subjects:
animal models
Animals
Aquaporin 4 - physiology
aquaporins
Astrocyte
astrocytes
Astrocytes - drug effects
Astrocytes - physiology
Biological and medical sciences
brain
Brain Chemistry - drug effects
Cell Adhesion - drug effects
connexins
Connexins - genetics
Connexins - physiology
Demyelinating Diseases - genetics
Demyelinating Diseases - pathology
Demyelinating Diseases - therapy
Development. Senescence. Regeneration. Transplantation
Fundamental and applied biological sciences. Psychology
Gap junction
genetically modified organisms
Glucose
Humans
Mice
mutation
Myelin
myelin sheath
Neuroglia - drug effects
Neurology
Oligodendrocyte
Oligodendroglia - drug effects
Oligodendroglia - physiology
Potassium
Potassium - physiology
Schwann cells
Vertebrates: nervous system and sense organs
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Summary:Abstract Several demyelinating syndromes have been linked to mutations in glial gap junction proteins, the connexins. Although mutations in connexins of the myelinating cells, Schwann cells and oligodendrocytes, were initially described, recent data have shown that astrocytes also play a major role in the demyelination process. Alterations in astrocytic proteins directly affect the oligodendrocytes’ ability to maintain myelin structure, and associated astrocytic proteins that regulate water and ionic fluxes, including aquaporins, can also regulate myelin integrity. Here, we will review the main evidence from human disorders and transgenic mouse models that implicate glial gap junction proteins in demyelinating diseases and the therapeutic potential of some of these targets. This article is part of a Special Issue entitled Electrical Synapses.
ISSN:0006-8993
1872-6240
DOI:10.1016/j.brainres.2012.07.003