The link between excitotoxic oligodendroglial death and demyelinating diseases
- PMID: 11250007
- DOI: 10.1016/s0166-2236(00)01746-x
The link between excitotoxic oligodendroglial death and demyelinating diseases
Abstract
Oligodendrocytes, the myelinating cells of CNS axons, are highly vulnerable to excitotoxic signals mediated by glutamate receptors of the AMPA and kainate classes. Receptors in these cells are commonly activated by glutamate that is released from axons and glial cells. In addition, oligodendrocytes contribute to the control of extracellular glutamate levels by means of their own transporters. However, acute and chronic alterations in glutamate homeostasis can result in overactivation of AMPA and kainate receptors and subsequent excitotoxic oligodendroglial death. Furthermore, demyelinating lesions caused by excitotoxins can be similar to those observed in multiple sclerosis. This, together with the effect of AMPA and kainate receptor antagonists in ameliorating the neurological score of animals with experimental autoimmune encephalomyelitis (an animal model of multiple sclerosis), indicates that oligodendrocyte excitotoxicity could be involved in the pathogenesis of demyelinating disorders.
Similar articles
-
Glutamate excitotoxicity--a mechanism for axonal damage and oligodendrocyte death in Multiple Sclerosis?J Neural Transm Suppl. 2000;(60):375-85. doi: 10.1007/978-3-7091-6301-6_27. J Neural Transm Suppl. 2000. PMID: 11205156
-
Excitotoxic oligodendrocyte death and axonal damage induced by glutamate transporter inhibition.Glia. 2005 Oct;52(1):36-46. doi: 10.1002/glia.20221. Glia. 2005. PMID: 15892126
-
AMPA and kainate receptors each mediate excitotoxicity in oligodendroglial cultures.Neurobiol Dis. 1999 Dec;6(6):475-85. doi: 10.1006/nbdi.1999.0264. Neurobiol Dis. 1999. PMID: 10600403
-
Glutamate receptors in neuroinflammatory demyelinating disease.Mediators Inflamm. 2006;2006(2):93684. doi: 10.1155/MI/2006/93684. Mediators Inflamm. 2006. PMID: 16883070 Free PMC article. Review.
-
Glutamate, T cells and multiple sclerosis.J Neural Transm (Vienna). 2017 Jul;124(7):775-798. doi: 10.1007/s00702-016-1661-z. Epub 2017 Feb 24. J Neural Transm (Vienna). 2017. PMID: 28236206 Review.
Cited by
-
Pathophysiology and neuroprotection of global and focal perinatal brain injury: lessons from animal models.Pediatr Neurol. 2015 Jun;52(6):566-584. doi: 10.1016/j.pediatrneurol.2015.01.016. Epub 2015 Jan 31. Pediatr Neurol. 2015. PMID: 26002050 Free PMC article. Review.
-
Oligodendrocyte N-methyl-D-aspartate receptor signaling: insights into its functions.Mol Neurobiol. 2013 Apr;47(2):845-56. doi: 10.1007/s12035-013-8408-8. Epub 2013 Jan 24. Mol Neurobiol. 2013. PMID: 23345133 Review.
-
Mechanisms Governing Oligodendrocyte Viability in Multiple Sclerosis and Its Animal Models.Cells. 2024 Jan 9;13(2):116. doi: 10.3390/cells13020116. Cells. 2024. PMID: 38247808 Free PMC article. Review.
-
Inflammation & apoptosis in spinal cord injury.Indian J Med Res. 2012 Mar;135(3):287-96. Indian J Med Res. 2012. PMID: 22561613 Free PMC article. Review.
-
TNFalpha-induced AMPA-receptor trafficking in CNS neurons; relevance to excitotoxicity?Neuron Glia Biol. 2004 Aug;1(3):263-73. doi: 10.1017/S1740925X05000608. Neuron Glia Biol. 2004. PMID: 16520832 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical