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Increased expression and function of glutamate transporters in multiple sclerosis
- Source :
- Neurobiology of Disease, Vol 21, Iss 1, Pp 154-164 (2006)
- Publication Year :
- 2006
- Publisher :
- Elsevier, 2006.
-
Abstract
- Recent studies have shown that glutamate excitotoxicity may be a component in the etiology of multiple sclerosis (MS). Glutamate transporters determine the levels of extracellular glutamate and are essential to prevent excitotoxicity. We have analyzed here the expression of the glutamate transporters EAAT1, EAAT2 and EAAT3 in control and in MS optic nerve samples. We observed an overall increase in the level of the glutamate transporters EAAT1 and EAAT2 mRNA and protein. In turn, functional assays showed that glutamate uptake was also increased in MS samples. Furthermore, glutamate transporter increases were mimicked in rat optic nerves treated with excitotoxic levels of glutamate. Together, these results indicate that enhanced expression of glutamate transporters in MS constitutes a regulatory response of glial cells to toxic levels of glutamate in the CNS during inflammation and neurodegeneration.
- Subjects :
- Adult
Male
Neurotoxins
Glutamate decarboxylase
Excitotoxicity
Glutamic Acid
Pharmacology
medicine.disease_cause
lcsh:RC321-571
Multiple sclerosis
Glutamate Plasma Membrane Transport Proteins
Glutamate aspartate transporter
medicine
Humans
RNA, Messenger
lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry
Aged
Oligonucleotide Array Sequence Analysis
Aged, 80 and over
biology
Chemistry
Oligodendrocytes
Metabotropic glutamate receptor 6
Glutamate receptor
Optic Nerve
Middle Aged
Excitatory Amino Acid Transporter 1
Oligodendroglia
Excitatory Amino Acid Transporter 3
Excitatory Amino Acid Transporter 2
Neurology
Biochemistry
Glutamate dehydrogenase 1
Metabotropic glutamate receptor
Astrocytes
Nerve Degeneration
biology.protein
NMDA receptor
Female
Glutamate
Subjects
Details
- Language :
- English
- Volume :
- 21
- Issue :
- 1
- Database :
- OpenAIRE
- Journal :
- Neurobiology of Disease
- Accession number :
- edsair.doi.dedup.....fc819e7f87c2f3247bd431ea7008a90d